ALBERT

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Ngang Heok Tang, Kyung Won Kim, Suhong Xu, Stephen M. Blazie, Brian A. Yee, Gene W. Yeo, Yishi Jin, Andrew D. Chisholm〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉mRNA decay factors regulate mRNA turnover by recruiting non-translating mRNAs and targeting them for translational repression and mRNA degradation. How mRNA decay pathways regulate cellular function 〈em〉in vivo〈/em〉 with specificity is poorly understood. Here, we show that 〈em〉C. elegans〈/em〉 mRNA decay factors, including the translational repressors CAR-1/LSM14 and CGH-1/DDX6, and the decapping enzymes DCAP-1/DCP1, function in neurons to differentially regulate axon development, maintenance, and regrowth following injury. In neuronal cell bodies, CAR-1 fully colocalizes with CGH-1 and partially colocalizes with DCAP-1, suggesting that mRNA decay components form at least two types of cytoplasmic granules. Following axon injury in adult neurons, loss of CAR-1 or CGH-1 results in increased axon regrowth and growth cone formation, whereas loss of DCAP-1 or DCAP-2 results in reduced regrowth. To determine how CAR-1 inhibits regrowth, we analyzed mRNAs bound to pan-neuronally expressed GFP::CAR-1 using a crosslinking and immunoprecipitation-based approach. Among the putative mRNA targets of CAR-1, we characterized the roles of 〈em〉micu-1〈/em〉, a regulator of the mitochondrial calcium uniporter MCU-1, in axon injury. We show that loss of 〈em〉car-1〈/em〉 results increased MICU-1 protein levels, and that enhanced axon regrowth in 〈em〉car-1〈/em〉 mutants is dependent on 〈em〉micu-1〈/em〉 and 〈em〉mcu-1.〈/em〉 Moreover, axon injury induces transient calcium influx into axonal mitochondria, dependent on MCU-1. In 〈em〉car-1〈/em〉 loss-of-function mutants and in 〈em〉micu-1〈/em〉 overexpressing animals, the axonal mitochondrial calcium influx is more sustained, which likely underlies enhanced axon regrowth. Our data uncover a novel pathway that controls axon regrowth through axonal mitochondrial calcium uptake.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S096098221931694X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Karin Kjernsmo, Heather M. Whitney, Nicholas E. Scott-Samuel, Joanna R. Hall, Henry Knowles, Laszlo Talas, Innes C. Cuthill〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Iridescence is a striking and taxonomically widespread form of animal coloration [1], but that its intense and varying hues could function as concealment [2] rather than signaling seems completely counterintuitive. Here, we show that the color changeability of biological iridescence, produced by multilayer cuticle reflectors in jewel beetle (〈em〉Sternocera aequisignata〈/em〉) wing cases, provides effective protection against predation by birds. Importantly, we also show that the most likely mechanism to explain this increase in survival is camouflage and not some other protective function, such as aposematism. In two field experiments using wild birds and humans, we measured both the “survival” and direct detectability of iridescent and non-iridescent beetle models and demonstrated that the iridescent treatment fared best in both experiments. We also show that an increased level of specular reflection (gloss) of the leaf background leads to an increase in the survival of all targets and, for detectability by humans, enhances the camouflage effect of iridescence. The latter suggests that some prey, particularly iridescent ones, can increase their chance of survival against visually hunting predators even further by choosing glossier backgrounds. Our study is the first to present direct empirical evidence that biological iridescence can work as a form of camouflage, providing an adaptive explanation for its taxonomically widespread occurrence.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Wilma A. Bainbridge, Chris I. Baker〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Boundary extension, a memory distortion in which observers consistently recall a scene with visual information beyond its boundaries, is widely accepted across the psychological sciences as a phenomenon revealing fundamental insight into memory representations [1, 2, 3], robust across paradigms [1, 4] and age groups [5, 6, 7]. This phenomenon has been taken to suggest that the mental representation of a scene consists of an intermingling of sensory information and a schema that extrapolates the views of a presented scene [8], and it has been used to provide evidence for the role of the neocortex [9] and hippocampus [10, 11] in the schematization of scenes during memory. However, the study of boundary extension has typically focused on object-oriented images that are not representative of our visuospatial world. Here, using a broad set of 1,000 images tested on 2,000 participants in a rapid recognition task, we discover “boundary contraction” as an equally robust phenomenon. Further, image composition largely drives whether extension or contraction is observed—although object-oriented images cause more boundary extension, scene-oriented images cause more boundary contraction. Finally, these effects also occur during drawing tasks, including a task with minimal memory load—when participants copy an image during viewing. Collectively, these results show that boundary extension is not a universal phenomenon and put into question the assumption that scene memory automatically combines visual information with additional context derived from internal schema. Instead, our memory for a scene may be largely driven by its visual composition, with a tendency to extend or contract the boundaries equally likely.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Ross G. Dwyer, Nils C. Krueck, Vinay Udyawer, Michelle R. Heupel, Demian Chapman, Harold L. Pratt, Ricardo Garla, Colin A. Simpfendorfer〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉No-take marine protected areas (MPAs) are a commonly applied tool to reduce human fishing impacts on marine and coastal ecosystems. However, conservation outcomes of MPAs for mobile and long-lived predators such as sharks are highly variable. Here, we use empirical animal tracking data from 459 individual sharks and baited remote underwater video surveys undertaken in 36 countries to construct an empirically supported individual-based model that estimates the conservation effectiveness of MPAs for five species of coral reef-associated sharks (〈em〉Triaenodon obesus〈/em〉, 〈em〉Carcharhinus melanopterus〈/em〉, 〈em〉Carcharhinus amblyrhynchos〈/em〉, 〈em〉Carcharhinus perezi〈/em〉, and 〈em〉Ginglymostoma cirratum〈/em〉). We demonstrate how species-specific individual movement traits can contribute to fishing mortality of sharks found within MPAs as they move outside to adjacent fishing grounds. We discovered that the world’s officially recorded coral reef-based managed areas (with a median width of 9.4 km) would need to be enforced as strict no-take MPAs and up to 5 times larger to expect protection of the majority of individuals of the five investigated reef shark species. The magnitude of this effect depended on local abundances and fishing pressure, with MPAs required to be 1.6–2.6 times larger to protect the same number of Atlantic and Caribbean species, which occur at lower abundances than similar species in the western Pacific. Furthermore, our model was used to quantify partially substantial reductions (〉50%) in fishing mortality resulting from small increases in MPA size, allowing us to bridge a critical gap between traditional conservation planning and fisheries management. Overall, our results highlight the challenge of relying on abundance data alone to ensure that estimates of shark conservation impacts of MPAs follow the precautionary approach.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Bryant E. Walker, Jaana Männik, Jaan Männik〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉During the early stages of cytokinesis, FtsZ protofilaments form a ring-like structure, the Z-ring, in most bacterial species. This cytoskeletal scaffold recruits downstream proteins essential for septal cell wall synthesis. Despite progress in understanding the dynamic nature of the Z-ring and its role in coordinating septal cell wall synthesis, the early stages of protofilament formation and subsequent assembly into the Z-ring are still not understood. Here we investigate a sequence of assembly steps that lead to the formation of the Z-ring in 〈em〉Escherichia coli〈/em〉 using high temporal and spatial resolution imaging. Our data show that formation of the Z-ring is preceded by transient membrane-linked FtsZ assemblies. These assemblies form after attachment of short cytosolic protofilaments, which we estimate to be less than 20 monomers long, to the membrane. The attachments occur at random locations along the length of the cell. The filaments treadmill and show periods of rapid growth and shrinkage. Their dynamic properties imply that protofilaments are bundled in these assemblies. Furthermore, we establish that the size of assemblies is sensitively controlled by the availability of FtsZ molecules and by the presence of ZapA proteins. The latter has been implicated in cross-linking the protofilaments. The likely function of these dynamic FtsZ assemblies is to sample the cell surface for the proper location for the Z-ring.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219316185-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Emma E. George, Filip Husnik, Daria Tashyreva, Galina Prokopchuk, Aleš Horák, Waldan K. Kwong, Julius Lukeš, Patrick J. Keeling〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Genome evolution in bacterial endosymbionts is notoriously extreme: the combined effects of strong genetic drift and unique selective pressures result in highly reduced genomes with distinctive adaptations to hosts [1, 2, 3, 4]. These processes are mostly known from animal endosymbionts, where nutritional endosymbioses represent the best-studied systems. However, eukaryotic microbes, or protists, also harbor diverse bacterial endosymbionts, but their genome reduction and functional relationships with their hosts are largely unexplored [5, 6, 7]. We sequenced the genomes of four bacterial endosymbionts from three species of diplonemids, poorly studied but abundant and diverse heterotrophic protists [8, 9, 10, 11, 12]. The endosymbionts come from two bacterial families, 〈em〉Rickettsiaceae〈/em〉 and 〈em〉Holosporaceae〈/em〉, that have invaded two families of diplonemids, and their genomes have converged on an extremely small size (605–632 kilobase pairs [kbp]), similar gene content (e.g., metabolite transporters and secretion systems), and reduced metabolic potential (e.g., loss of energy metabolism). These characteristics are generally found in both families, but the diplonemid endosymbionts have evolved greater extremes in parallel. They possess modified type VI secretion systems that could function in manipulating host metabolism or other intracellular interactions. Finally, modified cellular machinery like the ATP synthase without oxidative phosphorylation, and the reduced flagellar apparatus present in some diplonemid endosymbionts and nutritional animal endosymbionts, indicates that intracellular mechanisms have converged in bacterial endosymbionts with various functions and from different eukaryotic hosts across the tree of life.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Vani Narayanan, Laurel E. Schappell, Carl R. Mayer, Ashley A. Duke, Travis J. Armiger, Paul T. Arsenovic, Abhinav Mohan, Kris N. Dahl, Jason P. Gleghorn, Daniel E. Conway〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Epithelial cells spontaneously form acini (also known as cysts or spheroids) with a single, fluid-filled central lumen when grown in 3D matrices. The size of the lumen is dependent on apical secretion of chloride ions, most notably by the CFTR channel, which has been suggested to establish pressure in the lumen due to water influx. To study the cellular biomechanics of acini morphogenesis and homeostasis, we used MDCK-2 cells. Using FRET-force biosensors for E-cadherin, we observed significant increases in the average tension per molecule for each protein in mature 3D acini as compared to 2D monolayers. Increases in CFTR activity resulted in increased E-cadherin forces, indicating that ionic gradients affect cellular tension. Direct measurements of pressure revealed that mature acini experience significant internal hydrostatic pressure (37 ± 10.9 Pa). Changes in CFTR activity resulted in pressure and/or volume changes, both of which affect E-cadherin tension. Increases in CFTR chloride secretion also induced YAP signaling and cellular proliferation. In order to recapitulate disruption of acinar homeostasis, we induced epithelial-to-mesenchymal transition (EMT). During the initial stages of EMT, there was a gradual decrease in E-cadherin force and lumen pressure that correlated with lumen infilling. Strikingly, increasing CFTR activity was sufficient to block EMT. Our results show that ion secretion is an important regulator of morphogenesis and homeostasis in epithelial acini. Furthermore, this work demonstrates that, for closed 3D cellular systems, ion gradients can generate osmotic pressure or volume changes, both of which result in increased cellular tension.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219316203-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Kara K. Walker, Anne E. Pusey〈/p〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Juliane Uhlhorn, Mathias F. Wernet〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉A new study shows that the synaptically interconnected axon terminals of colour-sensitive fly photoreceptors that sample the same point in visual space receive additional inhibition from surrounding units; the resulting additional chromatic comparisons result in an optimal decorrelation of photoreceptor inputs. There are striking parallels between newly identified horizontal interactions and those mediated by mammalian horizontal cells.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Michael Gross〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Lineages changing their mode of locomotion are among the most conspicuous manifestations of evolutionary change. The appearance and disappearance of legs in events like the transition from fish to tetrapods, lizards to snakes, and tetrapods to whales has long fascinated biologists and lay people alike. Now genetics, developmental biology and paleontology are converging on a better understanding of these crucial transitions. 〈strong〉Michael Gross〈/strong〉 reports.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Francesco Monaca, Johannes Kohl〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉It remains unclear how hormonally mediated internal states affect specific brain circuits to modify behaviour. A new study reveals that a hypothalamic projection pathway critical for female sexual receptivity is extensively remodelled during the estrous cycle.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Sandra Citi〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Two recent studies report that ZO proteins, the main scaffolding proteins of tight junctions, undergo liquid phase separation. This new concept provides understanding at the mechanistic level of how tight junctions are formed and how they participate in mechanochemical signaling in early development.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): James D. Howard, Rachel Reynolds, Devyn E. Smith, Joel L. Voss, Geoffrey Schoenbaum, Thorsten Kahnt〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Outcome-guided behavior requires knowledge about the current value of expected outcomes. Such behavior can be isolated in the reinforcer devaluation task, which assesses the ability to infer the current value of specific rewards after devaluation. Animal lesion studies demonstrate that orbitofrontal cortex (OFC) is necessary for normal behavior in this task, but a causal role for human OFC in outcome-guided behavior has not been established. Here, we used sham-controlled, non-invasive, continuous theta-burst stimulation (cTBS) to temporarily disrupt human OFC network activity by stimulating a site in the lateral prefrontal cortex that is strongly connected to OFC prior to devaluation of food odor rewards. Subjects in the sham group appropriately avoided Pavlovian cues associated with devalued food odors. However, subjects in the stimulation group persistently chose those cues, even though devaluation of food odors themselves was unaffected by cTBS. This behavioral impairment was mirrored in changes in resting-state functional magnetic resonance imaging (rs-fMRI) activity such that subjects in the stimulation group exhibited reduced OFC network connectivity after cTBS, and the magnitude of this reduction was correlated with choices after devaluation. These findings demonstrate the feasibility of indirectly targeting the human OFC with non-invasive cTBS and indicate that OFC is specifically required for inferring the value of expected outcomes.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Chris MacDonald, S. Brookhart Shields, Charlotte A. Williams, Stanley Winistorfer, Robert C. Piper〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉In yeast, the main ubiquitin ligase responsible for the sorting of proteins to the lysosomal vacuole is Rsp5, a member of the Nedd4 family of ligases whose distinguishing features are a catalytic homologous to E6AP C terminus (HECT) domain and 3 central WW domains that bind PY motifs in target proteins. Many substrates do not bind Rsp5 directly and instead rely on PY-containing adaptor proteins that interact with Rsp5. Recent studies indicate that the activities of these adaptors are elevated when they undergo ubiquitination, yet the mechanism whereby ubiquitination activates the adaptors and how this process is regulated remain unclear. Here, we report on a mechanism that explains how ubiquitination stimulates adaptor function and how this process can be regulated by the Rsp5-associated deubiquitinase, Ubp2. Our overexpression experiments revealed that several adaptors compete for Rsp5 〈em〉in vivo〈/em〉. We found that the ability of the adaptors to compete effectively was enhanced by their ubiquitination and diminished by a block of their ubiquitination. Ubiquitination-dependent adaptor activation required a ubiquitin-binding surface within the Rsp5 catalytic HECT domain. Finally, like constitutively ubiquitinated adaptors, a Ubp2 deficiency increased both the adaptor activity and the ability to compete for Rsp5. Our data support a model whereby ubiquitinated Rsp5 adaptors are more active when “locked” onto Rsp5 via its N-lobe ubiquitin-binding surface and less active when they are “unlocked” by Ubp2-mediated deubiquitination.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S096098221931588X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Kristopher J. Kennedy, Michiko E. Taga〈/p〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Andrew Groover〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Sometimes the exceptions prove the rule, and lianas show some of the most exceptional stem anatomical variation in plants. New research describes the evolution and development of liana stem anatomical variants, and reveals new rules of woody growth.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Paloma Gonzalez-Bellido〈/p〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Goffredina Spanò, Frederik D. Weber, Gloria Pizzamiglio, Cornelia McCormick, Thomas D. Miller, Clive R. Rosenthal, Jamie O. Edgin, Eleanor A. Maguire〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The hippocampus plays a critical role in sleep-related memory processes [1, 2, 3], but it is unclear which specific sleep features are dependent upon this brain structure. The examination of sleep physiology in patients with focal bilateral hippocampal damage and amnesia could supply important evidence regarding these links. However, there is a dearth of such studies, despite these patients providing compelling insights into awake cognition [4, 5]. Here, we sought to identify the contribution of the hippocampus to the sleep phenotype by characterizing sleep via comprehensive qualitative and quantitative analyses in memory-impaired patients with selective bilateral hippocampal damage and matched control participants using in-home polysomnography on 4 nights. We found that, compared to control participants, patients had significantly reduced slow-wave sleep—likely due to decreased density of slow waves—as well as slow-wave activity. In contrast, slow and fast spindles were indistinguishable from those of control participants. Moreover, patients expressed slow oscillations (SOs), and SO-fast spindle coupling was observed. However, on closer scrutiny, we noted that the timing of spindles within the SO cycle was delayed in the patients. The shift of patients’ spindles into the later phase of the up-state within the SO cycle may indicate a mismatch in timing across the SO-spindle-ripple events that are associated with memory consolidation [6, 7]. The substantial effect of selective bilateral hippocampal damage on large-scale oscillatory activity in the cortex suggests that, as with awake cognition, the hippocampus plays a significant role in sleep physiology, which may, in turn, be necessary for efficacious episodic memory.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Jack A. Supple, Daniel Pinto-Benito, Christopher Khoo, Trevor J. Wardill, Samuel T. Fabian, Molly Liu, Siddhant Pusdekar, Daniel Galeano, Jintao Pan, Shengdian Jiang, Yimin Wang, Lijuan Liu, Hanchuan Peng, Robert M. Olberg, Paloma T. Gonzalez-Bellido〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Akin to all damselflies, 〈em〉Calopteryx〈/em〉 (family 〈em〉Calopterygidae〈/em〉), commonly known as jewel wings or demoiselles, possess dichoptic (separated) eyes with overlapping visual fields of view. In contrast, many dragonfly species possess holoptic (dorsally fused) eyes with limited binocular overlap. We have here compared the neuronal correlates of target tracking between damselfly and dragonfly sister lineages and linked these changes in visual overlap to pre-motor neural adaptations. Although dragonflies attack prey dorsally, we show that demoiselles attack prey frontally. We identify demoiselle target-selective descending neurons (TSDNs) with matching frontal visual receptive fields, anatomically and functionally homologous to the dorsally positioned dragonfly TSDNs. By manipulating visual input using eyepatches and prisms, we show that moving target information at the pre-motor level depends on binocular summation in demoiselles. Consequently, demoiselles encode directional information in a binocularly fused frame of reference such that information of a target moving toward the midline in the left eye is fused with information of the target moving away from the midline in the right eye. This contrasts with dragonfly TSDNs, where receptive fields possess a sharp midline boundary, confining responses to a single visual hemifield in a sagittal frame of reference (i.e., relative to the midline). Our results indicate that, although TSDNs are conserved across Odonata, their neural inputs, and thus the upstream organization of the target tracking system, differ significantly and match divergence in eye design and predatory strategies.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219316641-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Maria Makarova, Maria Peter, Gabor Balogh, Attila Glatz, James I. MacRae, Nestor Lopez Mora, Paula Booth, Eugene Makeyev, Laszlo Vigh, Snezhana Oliferenko〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Membrane function is fundamental to life. Each species explores membrane lipid diversity within a genetically predefined range of possibilities. How membrane lipid composition in turn defines the functional space available for evolution of membrane-centered processes remains largely unknown. We address this fundamental question using related fission yeasts 〈em〉Schizosaccharomyces pombe〈/em〉 and 〈em〉Schizo〈/em〉s〈em〉accharomyces〈/em〉 〈em〉japonicus〈/em〉. We show that, unlike 〈em〉S. pombe〈/em〉 that generates membranes where both glycerophospholipid acyl tails are predominantly 16–18 carbons long, 〈em〉S. japonicus〈/em〉 synthesizes unusual “asymmetrical” glycerophospholipids where the tails differ in length by 6–8 carbons. This results in stiffer bilayers with distinct lipid packing properties. Retroengineered 〈em〉S. pombe〈/em〉 synthesizing the 〈em〉S.〈/em〉-〈em〉japonicus〈/em〉-type phospholipids exhibits unfolded protein response and downregulates secretion. Importantly, our protein sequence comparisons and domain swap experiments support the hypothesis that transmembrane helices co-evolve with membranes, suggesting that, on the evolutionary scale, changes in membrane lipid composition may necessitate extensive adaptation of the membrane-associated proteome.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Alexander M.C. Bowles, Ulrike Bechtold, Jordi Paps〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Over the last 470 Ma, plant evolution has seen major evolutionary transitions, such as the move from water to land and the origins of vascular tissues, seeds, and flowers [1]. These have resulted in the evolution of terrestrial flora that has shaped modern ecosystems and the diversification of the Plant Kingdom, Viridiplantae, into over 374,000 described species [2]. Each of these transitions was accompanied by the gain and loss of genes in plant genomes. For example, whole-genome duplications are known to be fundamental to the origins of both seed and flowering plants [3, 4]. With the ever-increasing quality and quantity of whole-genome data, evolutionary insight into origins of distinct plant groups using comparative genomic techniques is now feasible. Here, using an evolutionary genomics pipeline to compare 208 complete genomes, we analyze the gene content of the ancestral genomes of the last common ancestor of land plants and all other major groups of plant. This approach reveals an unprecedented level of fundamental genomic novelties in two nodes related to the origin of land plants: the first in the origin of streptophytes during the Ediacaran and another in the ancestor of land plants in the Ordovician. Our findings highlight the biological processes that evolved with the origin of land plants and emphasize the importance of conserved gene novelties in plant diversification. Comparisons to other eukaryotic studies suggest a separation of the genomic origins of multicellularity and terrestrialization in plants.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315957-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Frederik S. Kamps, Jordan E. Pincus, Samaher F. Radwan, Stephanie Wahab, Daniel D. Dilks〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Human adults flawlessly and effortlessly navigate boundaries and obstacles in the immediately visible environment, a process we refer to as “visually guided navigation.” Neuroimaging work in adults suggests this ability involves the occipital place area (OPA) [1, 2]—a scene-selective region in the dorsal stream that selectively represents information necessary for visually guided navigation [3, 4, 5, 6, 7, 8, 9]. Despite progress in understanding the neural basis of visually guided navigation, however, little is known about how this system develops. Is navigationally relevant information processing present in the first few years of life? Or does this information processing only develop after many years of experience? Although a handful of studies have found selective responses to scenes (relative to objects) in OPA in childhood [10, 11, 12, 13], no study has explored how more specific navigationally relevant information processing emerges in this region. Here, we do just that by measuring OPA responses to first-person perspective motion information—a proxy for the visual experience of actually navigating the immediate environment—using fMRI in 5- and 8-year-old children. We found that, although OPA already responded more to scenes than objects by age 5, responses to first-person perspective motion were not yet detectable at this same age and rather only emerged by age 8. This protracted development was specific to first-person perspective motion through scenes, not motion on faces or objects, and was not found in other scene-selective regions (the parahippocampal place area or retrosplenial complex) or a motion-selective region (MT). These findings therefore suggest that navigationally relevant information processing in OPA undergoes prolonged development across childhood.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Ramya Lakshminarayan, Ben P. Phillips, Imogen L. Binnian, Natalia Gomez-Navarro, Norberto Escudero-Urquijo, Alan J. Warren, Elizabeth A. Miller〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Cells possess multiple mechanisms that protect against the accumulation of toxic aggregation-prone proteins. Here, we identify a pre-emptive pathway that reduces synthesis of membrane proteins that have failed to properly assemble in the endoplasmic reticulum (ER). We show that loss of the ER membrane complex (EMC) or mutation of the Sec61 translocon causes reduced synthesis of misfolded forms of the yeast ABC transporter Yor1. Synthesis defects are rescued by various ribosomal mutations, as well as by reducing cellular ribosome abundance. Genetic and biochemical evidence point to a ribosome-associated quality-control pathway triggered by ribosome collisions when membrane domain insertion and/or folding fails. In support of this model, translation initiation also contributes to synthesis defects, likely by modulating ribosome abundance on the message. Examination of translation efficiency across the yeast membrane proteome revealed that polytopic membrane proteins have relatively low ribosome abundance, providing evidence for translational tuning to balance protein synthesis and folding. We propose that by modulating translation rates of poorly folded proteins, cells can pre-emptively protect themselves from potentially toxic aberrant transmembrane proteins.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219316938-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Jun Young Heo, Min-Ho Nam, Hyung Ho Yoon, Jeongyeon Kim, Yu Jin Hwang, Woojin Won, Dong Ho Woo, Ji Ae Lee, Hyun-Jung Park, Seonmi Jo, Min Joung Lee, Sunpil Kim, Jeong-Eun Shim, Dong-Pyo Jang, Kyoung I. Kim, Sue H. Huh, Jae Y. Jeong, Neil W. Kowall, Junghee Lee, Hyeonjoo Im〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Current pharmacological treatments for Parkinson’s disease (PD) are focused on symptomatic relief, but not on disease modification, based on the strong belief that PD is caused by irreversible dopaminergic neuronal death. Thus, the concept of the presence of dormant dopaminergic neurons and its possibility as the disease-modifying therapeutic target against PD have not been explored. Here we show that optogenetic activation of substantia nigra pars compacta (SNpc) neurons alleviates parkinsonism in acute PD animal models by recovering tyrosine hydroxylase (TH) from the TH-negative dormant dopaminergic neurons, some of which still express DOPA decarboxylase (DDC). The TH loss depends on reduced dopaminergic neuronal firing under aberrant tonic inhibition, which is attributed to excessive astrocytic GABA. Blocking the astrocytic GABA synthesis recapitulates the therapeutic effect of optogenetic activation. Consistently, SNpc of postmortem PD patients shows a significant population of TH-negative/DDC-positive dormant neurons surrounded by numerous GABA-positive astrocytes. We propose that disinhibiting dormant dopaminergic neurons by blocking excessive astrocytic GABA could be an effective therapeutic strategy against PD.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315817-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 9 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Frank S. Heldt, John J. Tyson, Frederick R. Cross, Béla Novák〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Most eukaryotic cells execute binary division after each mass doubling in order to maintain size homeostasis by coordinating cell growth and division. By contrast, the photosynthetic green alga 〈em〉Chlamydomonas〈/em〉 can grow more than 8-fold during daytime and then, at night, undergo rapid cycles of DNA replication, mitosis, and cell division, producing up to 16 daughter cells. Here, we propose a mechanistic model for multiple-fission cycles and cell-size control in 〈em〉Chlamydomonas〈/em〉. The model comprises a light-sensitive and size-dependent biochemical toggle switch that acts as a sizer, guarding transitions into and exit from a phase of cell-division cycle oscillations. This simple “sizer-oscillator” arrangement reproduces the experimentally observed features of multiple-fission cycles and the response of 〈em〉Chlamydomonas〈/em〉 cells to different light-dark regimes. Our model also makes specific predictions about the size dependence of the time of onset of cell division after cells are transferred from light to dark conditions, and we confirm these predictions by single-cell experiments. Collectively, our results provide a new perspective on the concept of a “commitment point” during the growth of 〈em〉Chlamydomonas〈/em〉 cells and hint at intriguing similarities of cell-size control in different eukaryotic lineages.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219316215-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Désirée Brucks, Auguste M.P. von Bayern〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Helping others to obtain benefits, even at a cost to oneself, poses an evolutionary puzzle [1]. While kin selection explains such “selfless” acts among relatives, only reciprocity (paying back received favors) entails fitness benefits for unrelated individuals [2]. So far, experimental evidence for both prosocial helping (providing voluntary assistance for achieving an action-based goal) and reciprocity has been reported in a few mammals but no avian species [3]. In order to gain insights into the evolutionary origins of these behaviors, the capacity of non-mammalian species for prosociality and for reciprocity needs to be investigated. We tested two parrot species in an instrumental-helping paradigm involving “token transfer.” Here, actors could provide tokens to their neighbor, who could exchange them with an experimenter for food. To verify whether the parrots understood the task’s contingencies, we systematically varied the presence of a partner and the possibility for exchange. We found that African grey parrots voluntarily and spontaneously transferred tokens to conspecific partners, whereas significantly fewer transfers occurred in the control conditions. Transfers were affected by the strength of the dyads’ affiliation and partially by the receivers’ attention-getting behaviors. Furthermore, the birds reciprocated the help once the roles were reversed. Blue-headed macaws, in contrast, transferred hardly any tokens. Species differences in social tolerance might explain this discrepancy. These findings show that instrumental helping based on a prosocial attitude, accompanied but potentially not sustained by reciprocity, is present in parrots, suggesting that this capacity evolved convergently in this avian group and mammals.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Sarah L. Heath, Matthias P. Christenson, Elie Oriol, Maia Saavedra-Weisenhaus, Jessica R. Kohn, Rudy Behnia〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Spectral information is commonly processed in the brain through generation of antagonistic responses to different wavelengths. In many species, these color opponent signals arise as early as photoreceptor terminals. Here, we measure the spectral tuning of photoreceptors in 〈em〉Drosophila〈/em〉. In addition to a previously described pathway comparing wavelengths at each point in space, we find a horizontal-cell-mediated pathway similar to that found in mammals. This pathway enables additional spectral comparisons through lateral inhibition, expanding the range of chromatic encoding in the fly. Together, these two pathways enable efficient decorrelation and dimensionality reduction of photoreceptor signals while retaining maximal chromatic information. A biologically constrained model accounts for our findings and predicts a spatio-chromatic receptive field for fly photoreceptor outputs, with a color opponent center and broadband surround. This dual mechanism combines motifs of both an insect-specific visual circuit and an evolutionarily convergent circuit architecture, endowing flies with the ability to extract chromatic information at distinct spatial resolutions.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315775-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Scott R. Miller, Reid Longley, Patrick R. Hutchins, Thorsten Bauersachs〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Cellular innovation is central to biological diversification, yet its underlying mechanisms remain poorly understood [1]. One potential source of new cellular traits is environmentally induced phenotypic variation, or phenotypic plasticity. The plasticity-first hypothesis [2, 3, 4] proposes that natural selection can improve upon an ancestrally plastic phenotype to produce a locally adaptive trait, but the role of plasticity for adaptive evolution is still unclear [5, 6, 7, 8, 9, 10]. Here, we show that a structurally novel form of the heterocyst, the specialized nitrogen-fixing cell of the multicellular cyanobacterium 〈em〉Fischerella thermalis〈/em〉, has evolved multiple times from ancestrally plastic developmental variation during adaptation to high temperature. Heterocyst glycolipids (HGs) provide an extracellular gas diffusion barrier that protects oxygen-sensitive nitrogenase [11, 12], and cyanobacteria typically exhibit temperature-induced plasticity in HG composition that modulates heterocyst permeability [13, 14]. By contrast, high-temperature specialists of 〈em〉F. thermalis〈/em〉 constitutively overproduce glycolipid isomers associated with high temperature to levels unattained by plastic strains. This results in a less-permeable heterocyst, which is advantageous at high temperature but deleterious at low temperature for both nitrogen fixation activity and fitness. Our study illustrates how the origin of a novel cellular phenotype by the genetic assimilation and adaptive refinement of a plastic trait can be a source of biological diversity and contribute to ecological specialization.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Michael S. Drews, Aljoscha Leonhardt, Nadezhda Pirogova, Florian G. Richter, Anna Schuetzenberger, Lukas Braun, Etienne Serbe, Alexander Borst〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Sensory systems need to reliably extract information from highly variable natural signals. Flies, for instance, use optic flow to guide their course and are remarkably adept at estimating image velocity regardless of image statistics. Current circuit models, however, cannot account for this robustness. Here, we demonstrate that the 〈em〉Drosophila〈/em〉 visual system reduces input variability by rapidly adjusting its sensitivity to local contrast conditions. We exhaustively map functional properties of neurons in the motion detection circuit and find that local responses are compressed by surround contrast. The compressive signal is fast, integrates spatially, and derives from neural feedback. Training convolutional neural networks on estimating the velocity of natural stimuli shows that this dynamic signal compression can close the performance gap between model and organism. Overall, our work represents a comprehensive mechanistic account of how neural systems attain the robustness to carry out survival-critical tasks in challenging real-world environments.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Naoki Okamoto, Naoki Yamanaka〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Steroid hormones control various aspects of brain development and behavior in metazoans, but how they enter the central nervous system (CNS) through the blood-brain barrier (BBB) remains poorly understood. It is generally believed that steroid hormones freely diffuse through the plasma membrane of the BBB cells to reach the brain [1], because of the predominant “simple diffusion” model of steroid hormone transport across cell membranes. Recently, however, we challenged the simple diffusion model by showing that a 〈em〉Drosophila〈/em〉 organic anion-transporting polypeptide (OATP), which we named Ecdysone Importer (EcI), is required for cellular uptake of the primary insect steroid hormone ecdysone [2]. As ecdysone is first secreted into the hemolymph before reaching the CNS [3], our finding raised the question of how ecdysone enters the CNS through the BBB to exert its diverse role in 〈em〉Drosophila〈/em〉 brain development. Here, we demonstrate in the 〈em〉Drosophila〈/em〉 BBB that EcI is indispensable for ecdysone entry into the CNS to facilitate brain development. EcI is highly expressed in surface glial cells that form the BBB, and 〈em〉EcI〈/em〉 knockdown in the BBB suppresses ecdysone signaling within the CNS and blocks ecdysone-mediated neuronal events during development. In an 〈em〉ex vivo〈/em〉 culture system, the CNS requires EcI in the BBB to incorporate ecdysone from the culture medium. Our results suggest a transporter-mediated mechanism of steroid hormone entry into the CNS, which may provide important implications in controlling brain development and behavior by regulating steroid hormone permeability across the BBB.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315878-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Alan Brelsford, Jessica Purcell, Amaury Avril, Patrick Tran Van, Junxia Zhang, Timothée Brütsch, Liselotte Sundström, Heikki Helanterä, Michel Chapuisat〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Supergenes, clusters of tightly linked genes, play a key role in the evolution of complex adaptive variation [1, 2]. Although supergenes have been identified in many species, we lack an understanding of their origin, evolution, and persistence [3]. Here, we uncover 20–40 Ma of evolutionary history of a supergene associated with polymorphic social organization in 〈em〉Formica〈/em〉 ants [4]. We show that five 〈em〉Formica〈/em〉 species exhibit homologous divergent haplotypes spanning 11 Mbp on chromosome 3. Despite the supergene’s size, only 142 single nucleotide polymorphisms (SNPs) consistently distinguish alternative supergene haplotypes across all five species. These conserved 〈em〉trans〈/em〉-species SNPs are localized in a small number of disjunct clusters distributed across the supergene. This unexpected pattern of divergence indicates that the 〈em〉Formica〈/em〉 supergene does not follow standard models of sex chromosome evolution, in which distinct evolutionary strata reflect an expanding region of suppressed recombination [5]. We propose an alternative “eroded strata model” in which clusters of conserved 〈em〉trans〈/em〉-species SNPs represent functionally important areas maintained by selection in the face of rare recombination between ancestral haplotypes. The comparison of whole-genome sequences across 10 additional 〈em〉Formica〈/em〉 species reveals that the most conserved region of the supergene contains a transcription factor essential for motor neuron development in 〈em〉Drosophila〈/em〉 [6]. The discovery that a very small portion of this large and ancient supergene harbors conserved 〈em〉trans〈/em〉-species SNPs linked to colony social organization suggests that the ancestral haplotypes have been eroded by recombination, with selection preserving differentiation at one or a few genes generating alternative social organization.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Lauren Sumner-Rooney, John D. Kirwan, Elijah Lowe, Esther Ullrich-Lüter〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Almost all animals can sense light, but only those with spatial vision can “see.” Conventionally, this was restricted to animals possessing discrete visual organs (eyes), but extraocular vision could facilitate vision without eyes. Echinoderms form the focus of extraocular vision research [1, 2, 3, 4, 5, 6, 7], and the brittle star 〈em〉Ophiocoma wendtii〈/em〉, which exhibits light-responsive color change and shelter seeking, became a key species of interest [4, 8, 9]. Both 〈em〉O. wendtii〈/em〉 and an apparently light-indifferent congeneric, 〈em〉O. pumila〈/em〉, possess an extensive network of r-opsin-reactive cells, but its function remains unclear [4]. We show that, although both species are strongly light averse, 〈em〉O. wendtii〈/em〉 orients to stimuli necessitating spatial vision for detection, but 〈em〉O. pumila〈/em〉 does not. However, 〈em〉O. wendtii〈/em〉’s response disappears when chromatophores are contracted within the skeleton. Combining immunohistochemistry, histology, and synchrotron microtomography, we reconstructed models of photoreceptors 〈em〉in situ〈/em〉 and extracted estimated angular apertures for 〈em〉O. wendtii〈/em〉 and 〈em〉O. pumila〈/em〉. Angular sensitivity estimates, derived from these models, support the hypothesis that chromatophores constitute a screening mechanism in 〈em〉O. wendtii,〈/em〉 providing sufficient resolving power to detect the stimuli. RNA sequencing (RNA-seq) identified opsin candidates in both species, including multiple r-opsins and transduction pathway constituents, congruent with immunohistochemistry and studies of other echinoderms [10, 11]. Finally, we note that differing body postures between the two species during experiments may reflect aspect of signal integration. This represents one of the most detailed mechanisms for extraocular vision yet proposed and draws interesting parallels with the only other confirmed extraocular visual system, that of some sea urchins, which also possess chromatophores [1].〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Sridhar Ravi, Ryusuke Noda, Susie Gagliardi, Dmitry Kolomenskiy, Stacey Combes, Hao Liu, Andrew A. Biewener, Nicolai Konow〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Both biological and artificial fliers must contend with aerial perturbations that are ubiquitous in the outdoor environment. Flapping fliers are generally least stable but also most maneuverable around the roll axis, yet our knowledge of roll control in biological fliers remains limited. Hummingbirds are suitable models for linking aerodynamic perturbations to flight control strategies, as these small, powerful fliers are capable of remaining airborne even in adverse wind conditions. We challenged hummingbirds to fly within a steady, longitudinally (streamwise) oriented vortex that imposed a continuous roll perturbation, measured wing kinematics and neuromotor activation of the flight muscles with synchronized high-speed video and electromyography and used computational fluid dynamics (CFD) to estimate the aerodynamic forces generated by observed wing motions. Hummingbirds responded to the perturbation with bilateral differences in activation of the main flight muscles while maintaining symmetry in most major aspects of wing motion, including stroke amplitude, stroke plane angle, and flapping frequency. Hummingbirds did display consistent bilateral differences in subtler wing kinematic traits, including wing rotation and elevation. CFD modeling revealed that asymmetric wing rotation was critical for attenuating the effects of the perturbation. The birds also augmented flight stabilization by adjusting body and tail posture to expose greater surface area to upwash than to the undesirable downwash. Our results provide insight into the remarkable capacity of hummingbirds to maintain flight control, as well as bio-inspiration for simple yet effective control strategies that could allow robotic fliers to contend with unfamiliar and challenging real-world aerial conditions.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 2 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Hiroshi Ishimoto, Azusa Kamikouchi〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉In the early phase of courtship, female fruit flies exhibit an acute rejection response to avoid unfavorable mating. This pre-mating rejection response is evolutionarily paralleled across species, but the molecular and neuronal basis of that behavior is unclear. Here, we show that a putative incoherent feedforward circuit comprising ellipsoid body neurons, cholinergic R4d, and its repressor GABAergic R2/R4m neurons regulates the pre-mating rejection response in the virgin female 〈em〉Drosophila melanogaster〈/em〉. Both R4d and R2/R4m are positively regulated, via specific dopamine receptors, by a subset of neurons in the dopaminergic PPM3 cluster. Genetic deprivation of GABAergic signal via GABA〈sub〉A〈/sub〉 receptor RNA interference in this circuit induces a massive rejection response, whereas activation of GABAergic R2/R4m or suppression of cholinergic R4d increases receptivity. Moreover, glutamatergic signaling via 〈em〉N〈/em〉-methyl-〈span〉d〈/span〉-aspartate receptors induces NO-mediated retrograde regulation potentially from R4d to R2/R4m, likely providing flexible control of the behavioral switching from rejection to acceptance. Our study elucidates the molecular and neural mechanisms regulating the behavioral selection process of the pre-mating female.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Megan E.S. Sørensen, A. Jamie Wood, Ewan J.A. Minter, Chris D. Lowe, Duncan D. Cameron, Michael A. Brockhurst〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Through the merger of previously independent lineages, symbiosis promotes the acquisition of new traits and exploitation of inaccessible ecological niches [1, 2], driving evolutionary innovation and important ecosystem functions [3, 4, 5, 6]. The transient nature of establishment makes study of symbiotic origins difficult, but experimental comparison of independent origins could reveal the degree of convergence in the underpinning mechanisms [7, 8]. We compared the metabolic mechanisms of two independent origins of 〈em〉Paramecium bursaria-Chlorella〈/em〉 photosymbiosis [9, 10, 11] using a reciprocal metabolomic pulse-chase method. This showed convergent patterns of nutrient exchange and utilization for host-derived nitrogen in the 〈em〉Chlorella〈/em〉 genotypes [12, 13] and symbiont-derived carbon in the 〈em〉P. bursaria〈/em〉 genotypes [14, 15]. Consistent with a convergent primary nutrient exchange, partner-switched host-symbiont pairings were functional. Direct competition of hosts containing native or recombined symbionts against isogenic symbiont-free hosts showed that the fitness benefits of symbiosis for hosts increased with irradiance but varied by genotype. Global metabolism varied more between the 〈em〉Chlorella〈/em〉 than the 〈em〉P. bursaria〈/em〉 genotypes and suggested divergent mechanisms of light management. Specifically, the algal symbiont genotypes either produced photo-protective carotenoid pigments at high irradiance or more chlorophyll, resulting in corresponding differences in photosynthetic efficiency and non-photochemical quenching among host-symbiont pairings. These data suggest that the multiple origins of 〈em〉P. bursaria〈/em〉-〈em〉Chlorella〈/em〉 symbiosis use a convergent nutrient exchange, whereas other photosynthetic traits linked to functioning of photosymbiosis have diverged. Although convergence enables partner switching among diverse strains, phenotypic mismatches resulting from divergence of secondary symbiotic traits could mediate host-symbiont specificity in nature.〈/p〉〈/div〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Daniel A. Friess, Erik S. Yando, Guilherme M.O. Abuchahla, Janine B. Adams, Stefano Cannicci, Steven W.J. Canty, Kyle C. Cavanaugh, Rod M. Connolly, Nicole Cormier, Farid Dahdouh-Guebas, Karen Diele, Ilka C. Feller, Sara Fratini, Tim C. Jennerjahn, Shing Yip Lee, Danielle E. Ogurcak, Xiaoguang Ouyang, Kerrylee Rogers, Jennifer K. Rowntree, Sahadev Sharma〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Michael Tessler, Mercer R. Brugler, John A. Burns, Nina R. Sinatra, Daniel M. Vogt, Anand Varma, Madelyne Xiao, Robert J. Wood, David F. Gruber〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Michael Gross〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): John McCutcheon〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Larisa R.G. DeSantis, Robert S. Feranec, Kena Fox-Dobbs, John M. Harris, Thure E. Cerling, Jonathan M. Crites, Aisling B. Farrell, Gary T. Takeuchi〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Boris Worm〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Blaire Van Valkenburgh, Mark T. Clementz, Merav Ben-David〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Jesse Granger, Lucianne Walkowicz, Robert Fitak, Sönke Johnsen〈/p〉

Description: 〈p〉Publication date: Available online 13 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Iris Steitz, Manfred Ayasse〈/p〉

Description: 〈p〉Publication date: Available online 6 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Jordi Chan, Enrico Coen〈/p〉

Description: 〈p〉Publication date: Available online 7 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Ruddi Rodríguez-García, Vladimir A. Volkov, Chiung-Yi Chen, Eugene A. Katrukha, Natacha Olieric, Amol Aher, Ilya Grigoriev, Magdalena Preciado López, Michel O. Steinmetz, Lukas C. Kapitein, Gijsje Koenderink, Marileen Dogterom, Anna Akhmanova〈/p〉

Description: 〈p〉Publication date: Available online 7 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Andreia Cruz, Mirjam Heinemans, Cristina Márquez, Marta A. Moita〈/p〉

Description: 〈p〉Publication date: 3 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 3〈/p〉 〈p〉Author(s): Michael Gross〈/p〉

Description: 〈p〉Publication date: 3 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 3〈/p〉 〈p〉Author(s): Harmit Malik〈/p〉

Description: 〈p〉Publication date: 3 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 3〈/p〉 〈p〉Author(s): The Cell Press Team〈/p〉

Description: 〈p〉Publication date: 3 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 3〈/p〉 〈p〉Author(s): Loren J. Martin, Erinn L. Acland, Chulmin Cho, Wiebke Gandhi, Di Chen, Elizabeth Corley, Basil Kadoura, Tess Levy, Sara Mirali, Sarasa Tohyama, Sana Khan, Leigh C. MacIntyre, Erika N. Carlson, Petra Schweinhardt, Jeffrey S. Mogil〈/p〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): François M. Lambert, Julien Bacqué-Cazenave, Anne Le Seach, Jessica Arama, Gilles Courtand, Michele Tagliabue, Selim Eskiizmirliler, Hans Straka, Mathieu Beraneck〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Locomotor maturation requires concurrent gaze stabilization improvement for maintaining visual acuity [1, 2]. The capacity to stabilize gaze, in particular in small aquatic vertebrates where coordinated locomotor activity appears very early, is determined by assembly and functional maturation of inner ear structures and associated sensory-motor circuitries [3, 4, 5, 6, 7]. Whereas utriculo-ocular reflexes become functional immediately after hatching [8, 9], semicircular canal-dependent vestibulo-ocular reflexes (VORs) appear later [10]. Thus, small semicircular canals are unable to detect swimming-related head oscillations, despite the fact that corresponding acceleration components are well-suited to trigger an angular VOR [11]. This leaves the utricle as the sole vestibular origin for swimming-related compensatory eye movements [12, 13]. We report a remarkable ontogenetic plasticity of swimming-related head kinematics and vestibular end organ recruitment in 〈em〉Xenopus〈/em〉 tadpoles with beneficial consequences for gaze-stabilization. Swimming of older larvae generates sinusoidal head undulations with small, similar curvature angles on the left and right side that optimally activate horizontal semicircular canals. Young larvae swimming causes left-right head undulations with narrow curvatures and strong, bilaterally dissimilar centripetal acceleration components well suited to activate utricular hair cells and to substitute the absent semicircular canal function at this stage. The capacity of utricular signals to supplant semicircular canal function was confirmed by recordings of eye movements and extraocular motoneurons during off-center rotations in control and semicircular canal-deficient tadpoles. Strong alternating curvature angles and thus linear acceleration profiles during swimming in young larvae therefore represents a technically elegant solution to compensate for the incapacity of small semicircular canals to detect angular acceleration components.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S096098221931680X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Taiyo Toriba, Hiroki Tokunaga, Kazuma Nagasawa, Fanyu Nie, Akiko Yoshida, Junko Kyozuka〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Rhizomes are modified stems that grow horizontally underground in various perennial species, a growth habit that is advantageous for vigorous asexual proliferation. In 〈em〉Oryza longistaminata〈/em〉, a rhizomatous wild relative of cultivated rice (〈em〉Oryza sativa〈/em〉), leaves in the aerial shoots consist of a distal leaf blade and a proximal leaf sheath [1]. Leaf blade formation is, however, suppressed in rhizome leaves. In 〈em〉O. sativa〈/em〉, 〈em〉BLADE-ON-PETIOLE〈/em〉 (〈em〉BOP〈/em〉) genes are the main regulators of proximal-distal leaf patterning [2]. During the juvenile phase of 〈em〉O. sativa〈/em〉, 〈em〉BOP〈/em〉 expression is maintained at high levels by the small regulatory RNA microRNA156 (miR156), leading to formation of leaves consisting predominantly of the sheath. Here, we show that in 〈em〉O. longistaminata〈/em〉, high expression of 〈em〉BOP〈/em〉s caused by miR156 was responsible for suppression of the blade in rhizomes and that 〈em〉bop〈/em〉 loss-of-function mutants produced leaves consisting of the leaf blade only. Rhizome growth in soil was also hampered in the mutants due to a severe reduction in rhizome tip stiffness. Leaf blade formation is also suppressed in the stolons of 〈em〉Zoysia matrella〈/em〉, a monocot species, and in the rhizomes of 〈em〉Houttuynia cordata〈/em〉, a dicot species, indicating that leaf blade suppression is widely conserved. We also show that strong expression of 〈em〉BOP〈/em〉 homologs in both rhizome and stolon leaves rather than in aerial leaves is another conserved feature. We propose that suppression of the leaf blade by 〈em〉BOP〈/em〉 is an evolutionary strategy that has been commonly recruited by both rhizomatous and stoloniferous species to establish their unique growth habit.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Shutang Tan, Melinda Abas, Inge Verstraeten, Matouš Glanc, Gergely Molnár, Jakub Hajný, Pavel Lasák, Ivan Petřík, Eugenia Russinova, Jan Petrášek, Ondřej Novák, Jiří Pospíšil, Jiří Friml〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Plants, like other multicellular organisms, survive through a delicate balance between growth and defense against pathogens. Salicylic acid (SA) is a major defense signal in plants, and the perception mechanism as well as downstream signaling activating the immune response are known. Here, we identify a parallel SA signaling that mediates growth attenuation. SA directly binds to A subunits of protein phosphatase 2A (PP2A), inhibiting activity of this complex. Among PP2A targets, the PIN2 auxin transporter is hyperphosphorylated in response to SA, leading to changed activity of this important growth regulator. Accordingly, auxin transport and auxin-mediated root development, including growth, gravitropic response, and lateral root organogenesis, are inhibited. This study reveals how SA, besides activating immunity, concomitantly attenuates growth through crosstalk with the auxin distribution network. Further analysis of this dual role of SA and characterization of additional SA-regulated PP2A targets will provide further insights into mechanisms maintaining a balance between growth and defense.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315283-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Luca Cirillo, Adeline Cieren, Sofia Barbieri, Anthony Khong, Françoise Schwager, Roy Parker, Monica Gotta〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Stress granules (SGs) are membraneless organelles that form in eukaryotic cells after stress exposure [1] (reviewed in [2, 3, 4]). Following translation inhibition, polysome disassembly releases 48S preinitiation complexes (PICs). mRNA, PICs, and other proteins coalesce in SG cores [1, 5, 6, 7]. SG cores recruit a dynamic shell, whose properties are dominated by weak interactions between proteins and RNAs [8, 9, 10]. The structure and assembly of SGs and how different components contribute to their formation are not fully understood. Using super-resolution and expansion microscopy, we find that the SG component UBAP2L [11, 12] and the core protein G3BP1 [5, 11, 12, 13] occupy different domains inside SGs. UBAP2L displays typical properties of a core protein, indicating that cores of different compositions coexist inside the same granule. Consistent with a role as a core protein, UBAP2L is required for SG assembly in several stress conditions. Our reverse genetic and cell biology experiments suggest that UBAP2L forms granules independent of G3BP1 and 2 but does not interfere with stress-induced translational inhibition. We propose a model in which UBAP2L is an essential SG nucleator that acts upstream of G3BP1 and 2 and facilitates G3BP1 core formation and SG assembly and growth.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S096098221931615X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Sacha Escamez, Domenique André, Bernadette Sztojka, Benjamin Bollhöner, Hardy Hall, Béatrice Berthet, Ute Voß, Amnon Lers, Alexis Maizel, Magnus Andersson, Malcolm Bennett, Hannele Tuominen〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Plant organ growth is widely accepted to be determined by cell division and cell expansion, but, unlike that in animals, the contribution of cell elimination has rarely been recognized. We investigated this paradigm during 〈em〉Arabidopsis〈/em〉 lateral root formation, when the lateral root primordia (LRP) must traverse three overlying cell layers within the parent root. A subset of LRP-overlying cells displayed the induction of marker genes for cell types undergoing developmental cell death, and their cell death was detected by electron, confocal, and light sheet microscopy techniques. LRP growth was delayed in cell-death-deficient mutants lacking the positive cell death regulator ORESARA1/ANAC092 (ORE1). LRP growth was restored in 〈em〉ore1-2〈/em〉 knockout plants by genetically inducing cell elimination in cells overlying the LRP or by physically killing LRP-overlying cells by ablation with optical tweezers. Our results support that, in addition to previously discovered mechanisms, cell elimination contributes to regulating lateral root emergence.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315805-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 9 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Courtney E. Coombes, Harriet A.J. Saunders, Anirudh G. Mannava, Dena M. Johnson-Schlitz, Taylor A. Reid, Sneha Parmar, Mark McClellan, Connie Yan, Stephen L. Rogers, Jay Z. Parrish, Michael Wagenbach, Linda Wordeman, Jill Wildonger, Melissa K. Gardner〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Neuronal axons terminate as synaptic boutons that form stable yet plastic connections with their targets. Synaptic bouton development relies on an underlying network of both long-lived and dynamic microtubules that provide structural stability for the boutons while also allowing for their growth and remodeling. However, a molecular-scale mechanism that explains how neurons appropriately balance these two microtubule populations remains a mystery. We hypothesized that α-tubulin acetyltransferase (αTAT), which both stabilizes long-lived microtubules against mechanical stress via acetylation and has been implicated in promoting microtubule dynamics, could play a role in this process. Using the 〈em〉Drosophila〈/em〉 neuromuscular junction as a model, we found that non-enzymatic dαTAT activity limits the growth of synaptic boutons by affecting dynamic, but not stable, microtubules. Loss of dαTAT results in the formation of ectopic boutons. These ectopic boutons can be similarly suppressed by resupplying enzyme-inactive dαTAT or by treatment with a low concentration of the microtubule-targeting agent vinblastine, which acts to suppress microtubule dynamics. Biophysical reconstitution experiments revealed that non-enzymatic αTAT1 activity destabilizes dynamic microtubules but does not substantially impact the stability of long-lived microtubules. Further, during microtubule growth, non-enzymatic αTAT1 activity results in increasingly extended tip structures, consistent with an increased rate of acceleration of catastrophe frequency with microtubule age, perhaps via tip structure remodeling. Through these mechanisms, αTAT enriches for stable microtubules at the expense of dynamic ones. We propose that the specific suppression of dynamic microtubules by non-enzymatic αTAT activity regulates the remodeling of microtubule networks during synaptic bouton development.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Catherine A. Matulis, Juyue Chen, Aneysis D. Gonzalez-Suarez, Rudy Behnia, Damon A. Clark〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉In visual systems, neurons adapt both to the mean light level and to the range of light levels, or the contrast. Contrast adaptation has been studied extensively, but it remains unclear how it is distributed among neurons in connected circuits, and how early adaptation affects subsequent computations. Here, we investigated temporal contrast adaptation in neurons across 〈em〉Drosophila〈/em〉’s visual motion circuitry. Several ON-pathway neurons showed strong adaptation to changes in contrast over time. One of these neurons, Mi1, showed almost complete adaptation on fast timescales, and experiments ruled out several potential mechanisms for its adaptive properties. When contrast adaptation reduced the gain in ON-pathway cells, it was accompanied by decreased motion responses in downstream direction-selective cells. Simulations show that contrast adaptation can substantially improve motion estimates in natural scenes. The benefits are larger for ON-pathway adaptation, which helps explain the heterogeneous distribution of contrast adaptation in these circuits.〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Antonella Ruggiero, Yuki Katou, Katsuhiko Shirahige, Martial Séveno, Simonetta Piatti〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Accurate chromosome segregation requires bipolar attachment of kinetochores to spindle microtubules. A conserved surveillance mechanism, the spindle assembly checkpoint (SAC), responds to lack of kinetochore-microtubule connections and delays anaphase onset until all chromosomes are bipolarly attached [1]. SAC signaling fires at kinetochores and involves a soluble mitotic checkpoint complex (MCC) that inhibits the anaphase-promoting complex (APC) [2, 3]. The mitotic delay imposed by SAC, however, is not everlasting. If kinetochores fail to establish bipolar connections, cells can escape from the SAC-induced mitotic arrest through a process called mitotic slippage [4]. Mitotic slippage occurs in the presence of SAC signaling at kinetochores [5, 6], but whether and how MCC stability and APC inhibition are actively controlled during slippage is unknown. The PP1 phosphatase has emerged as a key factor in SAC silencing once all kinetochores are bipolarly attached [7, 8]. PP1 turns off SAC signaling through dephosphorylation of the SAC scaffold Knl1/Blinkin at kinetochores [9, 10, 11]. Here, we show that, in budding yeast, PP1 is also required for mitotic slippage. However, its involvement in this process is not linked to kinetochores but rather to MCC stability. We identify S268 of Mad3 as a critical target of PP1 in this process. Mad3 S268 dephosphorylation destabilizes the MCC without affecting the initial SAC-induced mitotic arrest. Conversely, it accelerates mitotic slippage and overcomes the slippage defect of PP1 mutants. Thus, slippage is not the mere consequence of incomplete APC inactivation that brings about mitotic exit, as originally proposed, but involves the exertive antagonism between kinases and phosphatases.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315246-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Melina Tsitsiklis, Jonathan Miller, Salman E. Qasim, Cory S. Inman, Robert E. Gross, Jon T. Willie, Elliot H. Smith, Sameer A. Sheth, Catherine A. Schevon, Michael R. Sperling, Ashwini Sharan, Joel M. Stein, Joshua Jacobs〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The hippocampus and surrounding medial-temporal-lobe (MTL) structures are critical for both memory and spatial navigation, but we do not fully understand the neuronal representations used to support these behaviors. Much research has examined how the MTL neurally represents spatial information, such as with “place cells” that represent an animal’s current location or “head-direction cells” that code for an animal’s current heading. In addition to behaviors that require an animal to attend to the current spatial location, navigating to remote destinations is a common part of daily life. To examine the neural basis of these behaviors, we recorded single-neuron activity from neurosurgical patients playing Treasure Hunt, a virtual-reality spatial-memory task. By analyzing how the activity of these neurons related to behavior in Treasure Hunt, we found that the firing rates of many MTL neurons during navigation significantly changed depending on the position of the current spatial target. In addition, we observed neurons whose firing rates during navigation were tuned to specific heading directions in the environment, and others whose activity changed depending on the timing within the trial. By showing that neurons in our task represent remote locations rather than the subject’s own position, our results suggest that the human MTL can represent remote spatial information according to task demands.〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 2 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Jocelyn F. Krey, Paroma Chatterjee, Rachel A. Dumont, Mary O’Sullivan, Dongseok Choi, Jonathan E. Bird, Peter G. Barr-Gillespie〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Actin-rich structures, like stereocilia and microvilli, are assembled with precise control of length, diameter, and relative spacing. By quantifying actin-core dimensions of stereocilia from phalloidin-labeled mouse cochleas, we demonstrated that inner hair cell stereocilia developed in specific stages, where a widening phase is sandwiched between two lengthening phases. Moreover, widening of the second-tallest stereocilia rank (row 2) occurred simultaneously with the appearance of mechanotransduction. Correspondingly, 〈em〉Tmc1〈/em〉〈sup〉KO/KO〈/sup〉;〈em〉Tmc2〈/em〉〈sup〉KO/KO〈/sup〉 or 〈em〉Tmie〈/em〉〈sup〉KO/KO〈/sup〉 hair cells, which lack transduction, have significantly altered stereocilia lengths and diameters, including a narrowed row 2. EPS8 and the short splice isoform of MYO15A, identity markers for mature row 1 (the tallest row), lost their row exclusivity in transduction mutants. GNAI3, another member of the mature row 1 complex, accumulated at mutant row 1 tips at considerably lower levels than in wild-type bundles. Alterations in stereocilia dimensions and in EPS8 distribution seen in transduction mutants were mimicked by block of transduction channels of cochlear explants in culture. In addition, proteins normally concentrated at mature row 2 tips were also distributed differently in transduction mutants; the heterodimeric capping protein subunit CAPZB and its partner TWF2 never concentrated at row 2 tips like they do in wild-type bundles. The altered distribution of marker proteins in transduction mutants was accompanied by increased variability in stereocilia length. Transduction channels thus specify and maintain row identity, control addition of new actin filaments to increase stereocilia diameter, and coordinate stereocilia height within rows.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315787-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 2 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Hironori Abe, Kris G. Alavattam, Yueh-Chiang Hu, Qishen Pang, Paul R. Andreassen, Rashmi S. Hegde, Satoshi H. Namekawa〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Meiotic sex chromosome inactivation (MSCI) is an essential event in the mammalian male germline. MSCI is directed by a DNA damage response (DDR) pathway centered on the phosphorylation of histone variant H2AX at serine 139 (termed γH2AX). The failure to initiate MSCI is linked to complete meiotic arrest and elimination of germ cells; however, the mechanisms underlying this arrest and elimination remain unknown. To address this question, we established a new separation-of-function mouse model for 〈em〉H2ax〈/em〉 that shows specific and complete defects in MSCI. The genetic change is a point mutation in which another H2AX amino acid residue important in the DDR, tyrosine 142 (Y142), is converted to alanine (〈em〉H2ax-Y142A〈/em〉). In 〈em〉H2ax-Y142A〈/em〉 meiosis, the establishment of DDR signals on the chromosome-wide domain of the sex chromosomes is impaired. The initiation of MSCI is required for stage progression, which enables crossover formation, suggesting that the establishment of MSCI permits the timely progression of male meiosis. Our results suggest that normal meiotic progression requires the removal of ATR-mediated DDR signaling from autosomes. We propose a novel biological function for MSCI: the initiation of MSCI sequesters DDR factors from autosomes to the sex chromosomes at the onset of the pachytene stage, and the subsequent formation of an isolated XY nuclear compartment—the XY body—sequesters DDR factors to permit meiotic progression from the mid-pachytene stage onward.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315660-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Eva L. Kozak, Subarna Palit, Jerónimo R. Miranda-Rodríguez, Aleksandar Janjic, Anika Böttcher, Heiko Lickert, Wolfgang Enard, Fabian J. Theis, Hernán López-Schier〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Chia-Hsuan Wang, Joseph D. Monaco, James J. Knierim〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Richard J. Howard, Xianguang Hou, Gregory D. Edgecombe, Tobias Salge, Xiaomei Shi, Xiaoya Ma〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Pierre Gautrat, Carole Laffont, Florian Frugier〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Clare R. Gamlin, Chi Zhang, Michael A. Dyer, Rachel O.L. Wong〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Ying Tan, Matthew Barnbrook, Yvette Wilson, Attila Molnár, Alfredas Bukys, Andrew Hudson〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Moumita Srivastava, Anjil K. Srivastava, Beatriz Orosa-Puente, Alberto Campanaro, Cunjin Zhang, Ari Sadanandom〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Roma Siugzdaite, Joe Bathelt, Joni Holmes, Duncan E. Astle〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Carlos Frederico Deluqui Gurgel, Olga Camacho, Antoine J.P. Minne, Thomas Wernberg, Melinda A. Coleman〈/p〉

Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Youbao Zhao, Yina Wang, Srijana Upadhyay, Chaoyang Xue, Xiaorong Lin〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Sara Letzner, Onur Güntürkün, Christian Beste〈/p〉

Description: 〈p〉Publication date: 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 4〈/p〉 〈p〉Author(s): Marjorie R. Lundgren, David L. Des Marais〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Shu-Chen Guan, Sheng-Hui Zhang, Yu-Cheng Zhang, Shi-Ming Tang, Cong Yu〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Nicolas M. Doll, Simone Bovio, Angelo Gaiti, Anne-Charlotte Marsollier, Sophy Chamot, Steven Moussu, Thomas Widiez, Gwyneth Ingram〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Kerstin Schäfer, Patrick Künzler, Andreas Klingl, Holger Eubel, Chris Carrie〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Sara S. Patterson, James A. Kuchenbecker, James R. Anderson, Maureen Neitz, Jay Neitz〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Adeline Orts-Del’Immagine, Yasmine Cantaut-Belarif, Olivier Thouvenin, Julian Roussel, Asha Baskaran, Dominique Langui, Fanny Koëth, Paul Bivas, François-Xavier Lejeune, Pierre-Luc Bardet, Claire Wyart〈/p〉

Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Anthony Dudilot, Emilie Trillaud-Doppia, Jannic Boehm〈/p〉

Description: 〈p〉Publication date: Available online 13 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Heidi A. Arjes, Lam Vo, Caroline M. Dunn, Lisa Willis, Christopher A. DeRosa, Cassandra L. Fraser, Daniel B. Kearns, Kerwyn Casey Huang〈/p〉

Description: 〈p〉Publication date: Available online 13 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Chih-Ying Lee, C. Gaston Bisig, Michael M. Conrad, Yanina Ditamo, Luciana Previato de Almeida, Michael E. Dresser, Roberto J. Pezza〈/p〉

Description: 〈p〉Publication date: Available online 13 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology〈/p〉 〈p〉Author(s): Hongjie Li, Tongchao Li, Felix Horns, Jiefu Li, Qijing Xie, Chuanyun Xu, Bing Wu, Justus M. Kebschull, Colleen N. McLaughlin, Sai Saroja Kolluru, Robert C. Jones, David Vacek, Anthony Xie, David J. Luginbuhl, Stephen R. Quake, Liqun Luo〈/p〉

Description: 〈p〉Publication date: 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 2〈/p〉 〈p〉Author(s): Erik G. Schad, Christian P. Petersen〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Regeneration involves regulating tissue proportionality across considerable size ranges through unknown mechanisms. In planarians, which scale reversibly over 40× through regeneration, we identify the Striatin-interacting phosphatase and kinase (STRIPAK) complex as a potent negative regulator of axis length. Inhibition of two proteins in the STRIPAK complex, 〈em〉mob4〈/em〉 and 〈em〉striatin〈/em〉, dramatically increased posterior length, through expansion of a posterior 〈em〉wnt1+〈/em〉 signaling center within midline muscle cells. 〈em〉wnt1〈/em〉 was required for tail expansion after 〈em〉mob4〈/em〉 inhibition and dynamically reestablishes proportionality after amputation in normal animals, indicating STRIPAK represses Wnt signaling for scaling. Regulation of 〈em〉wnt1〈/em〉 expansion was stem cell dependent, demonstrating that control of signaling-center production through stem cell differentiation underlies proportional growth in adult regenerative tissue.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0960982219315702-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Spencer A. Freeman, Sergio Grinstein〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The forces driving membrane protrusion during phagocytosis are poorly understood. A recent study describes how integrins in the phagocyte membrane provide a molecular clutch to enable the exertion of force by actin polymerizing at the leading edge of the pseudopods. These results explain the mechanosensitivity of phagocytic cells.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Pilar Cubas〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉How do perennial plants adapt their growth to seasonal changes? A new study in the hybrid aspen reveals that, in short days, repression of a growth-promoting genetic pathway leads to upregulation of the 〈em〉BRANCHED1〈/em〉 genes, which in turn induce growth cessation.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Robert M. Pringle〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Reconstructing prehistoric animal communities is important for understanding the emergence of modern ecosystems and the environmental context of human evolution. A new study of African fossils spanning seven million years shows that ancient large-herbivore assemblages were functionally distinct from those that exist today.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Roger B.J. Benson, Paul M. Barrett〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Plant-eating dinosaurs evolved varied feeding strategies. A new study demonstrates convergent evolution of their skulls and teeth towards two distinct functional optima, one resembling advanced mammalian herbivory and the other echoing herbivory in birds and other reptiles.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Ewa Chrostek, Gregory D.D. Hurst, Elizabeth A. McGraw〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Vector-borne viral diseases pose an urgent public health challenge, particularly in the tropics. Field releases of mosquitoes carrying bacterial symbionts that reduce vector competence are ongoing in Kuala Lumpur, Malaysia. Early results show that 〈em〉w〈/em〉AlbB 〈em〉Wolbachia〈/em〉 can persist in mosquitoes in urban settings and decrease dengue incidence in humans.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Mark S. Blumberg, John A. Lesku, Paul-Antoine Libourel, Markus H. Schmidt, Niels C. Rattenborg〈/p〉 〈div〉〈p〉For many decades, sleep researchers have sought to determine which species ‘have’ rapid eye movement (REM) sleep. In doing so, they relied predominantly on a template derived from the expression of REM sleep in the adults of a small number of mammalian species. Here, we argue for a different approach that focuses less on a binary decision about haves and have nots, and more on the diverse expression of REM sleep components over development and across species. By focusing on the components of REM sleep and discouraging continued reliance on a restricted template, we aim to promote a richer and more biologically grounded developmental–comparative approach that spans behavioral, physiological, neural, and ecological domains.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Susanne Schilling, Rainer Melzer, Paul F. McCabe〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Franklin Caval-Holme, Marla B. Feller〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): David Magnan, Mohan C. Joshi, Anna K. Barker, Bryan J. Visser, David Bates〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Thomas Richards〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Lee M. Henry, Jean Peccoud, Jean-Christophe Simon, Jarrod D. Hadfield, Martin J.C. Maiden, Julia Ferrari, H. Charles J. Godfray〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): John Pannell〈/p〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Veit Stuphorn〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Classically, specific orbitofrontal cortex (OFC) neurons are thought to represent attributes of specific decision options. A new model proposes instead that OFC neurons represent whichever option is currently attended. A recent study, however, tests these two models and rules out the ‘current-focus-of-attention’ model.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Michael Gross〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Human activities are shaping the biosphere pervasively, which has led to the concept of the Anthropocene. Although we are already causing a mass extinction, life on Earth is likely to survive for more than a billion years after our species has disappeared. 〈strong〉Michael Gross〈/strong〉 reports.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Giovanni Galizia〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Finding the right lure for trapping pest insects is difficult. The typical smell of rain and humid soil, geosmin, now turns out to be a strong attractant for the yellow fever mosquito 〈em〉Aedes aegypti〈/em〉.〈/p〉〈/div〉

Description: 〈p〉Publication date: 6 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Current Biology, Volume 30, Issue 1〈/p〉 〈p〉Author(s): Dena S. Goldblatt, David Schoppik〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Animals must distinguish external stimuli from self-generated sensory input to guide appropriate behaviors. A recent study elucidates a cellular mechanism by which zebrafish perform this distinction while maintaining sensitivity to external environmental signals.〈/p〉〈/div〉