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  • 1
    Publication Date: 2016-01-23
    Description: Fisheries management operates in an environment characterized by multiple risks. These risks are often complementary and can be traded off against each other. An important goal for managers is to develop strategies to minimize the overall risk exposure at minimal cost. We show a simple model that quantifies a range of risks faced by fisheries management agencies in terms of long-term expected budgetary expenditure. The model includes not only the cost a management agency would be expected to incur from overfishing a stock, or from being seen to overfish it, but also the social cost incurred from not achieving its objectives, such as the opportunity cost of foregoing catches and economic returns. These costs can be controlled by adjusting the biomass level targeted by management, or increasing expenditures for data collection to improve the precision of biomass estimates. The overall risk, expressed as the long-term total expected cost to a management agency, depends strongly on the fisheries management objectives, and the emphasis on conservation or economic motives. In general, management under a conservation-oriented objective would reduce risk either by increasing target biomass levels or by expenditure on monitoring and assessment, while a catch-focused objective would seek to lower management costs by reducing expenditure on data collection and assessment. Increased natural stock variability affects the risk of overfishing, and long-term expected costs as the ability to make a meaningful estimate of biomass declines. Management of catch-focused fisheries would reduce the biomass target as stock variability increases, because the benefit of catches are seen to outweigh the cost, or risk of being overfished. The model provides the basis for more extensive risk analyses, and serves as a simple lesson that the consequences of reducing the short-term costs associated with managing a fishery can come with a concomitant increase in overall risk.
    Print ISSN: 1054-3139
    Electronic ISSN: 1095-9289
    Topics: Biology , Geosciences , Physics
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  • 2
    Publication Date: 2012-07-28
    Description: FIG4 is a ubiquitously expressed phosphatase that, in complex with FAB1/PIKFYVE and VAC14, regulates the biosynthesis of the signaling lipid PI(3,5)P 2 . Null mutation of Fig4 in the mouse results in spongiform degeneration of brain and peripheral ganglia, defective myelination and juvenile lethality. Partial loss-of-function of human FIG4 results in a severe form of Charcot–Marie–Tooth neuropathy. Neurons from null mice contain enlarged vacuoles derived from the endosome/lysosome pathway, and astrocytes accumulate proteins involved in autophagy. Other cellular defects include astrogliosis and microgliosis. To distinguish the contributions of neurons and glia to spongiform degeneration in the Fig4 null mouse, we expressed Fig4 under the control of the neuron-specific enolase promoter and the astrocyte-specific glial fibrillary acidic protein promoter in transgenic mice. Neuronal expression of Fig4 was sufficient to rescue cellular and neurological phenotypes including spongiform degeneration, gliosis and juvenile lethality. In contrast, expression of Fig4 in astrocytes prevented accumulation of autophagy markers and microgliosis but did not prevent spongiform degeneration or lethality. To confirm the neuronal origin of spongiform degeneration, we generated a floxed allele of Fig4 and crossed it with mice expressing the Cre recombinase from the neuron-specific synapsin promoter. Mice with conditional inactivation of Fig4 in neurons developed spongiform degeneration and the full spectrum of neurological abnormalities. The data demonstrate that expression of Fig4 in neurons is necessary and sufficient to prevent spongiform degeneration. Therapy for patients with FIG4 deficiency will therefore require correction of the deficiency in neurons.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 3
    Publication Date: 2014-08-03
    Description: Duchenne muscular dystrophy (DMD) is a common and relentlessly progressive muscle disease. Some interventions have been identified that modestly slow progression and prolong survival, but more meaningful therapies are lacking. The goal of this study is to identify new therapeutic pathways for DMD using a zebrafish model of the disease. To accomplish this, we performed a non-biased drug screen in sapje , a zebrafish line with a recessive nonsense mutation in dystrophin. We identified 6 positive hits (out of 640 total drugs tested) by their ability to prevent abnormal birefringence in sapje . Follow-up analyses demonstrated that fluoxetine, a selective serotonin reuptake inhibitor (SSRI), provided the most substantial benefit. Morpholino-based experimentation confirmed that modulation of the serotonin pathway alone can prevent the dystrophic phenotype, and transcriptomic analysis revealed changes in calcium homeostasis as a potential mechanism. In all, we demonstrate that monoamine agonists can prevent disease in a vertebrate model of DMD. Given the safe and widespread use of SSRIs in clinical practice, our study identifies an attractive target pathway for therapy development.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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  • 4
    Publication Date: 2016-01-20
    Description: Individuals within social groups commonly combine vocal signals, forming duets. Although these displays have been described across taxa, their function is not fully understood. In birds, territory defense is a well-supported function of duetting, but additional functions are likely. Extrapair paternity (EPP) is common in birds, and males at risk of cuckoldry are expected to guard paternity in many ways, possibly including acoustic guarding with duets. Theoretical models predict species with moderate-to-high EPP rates will invest most in paternity-guarding, yet few studies have investigated duet function in such species. We conducted a dual-speaker playback experiment to test duet function in the red-backed fairy-wren, Malurus melanocephalus , which has moderately high EPP rates. Breeding groups were presented with 3 playback treatments: male solo, female solo, and duet. The territory defense hypothesis predicts pairs will respond aggressively and sing duets during duet playback in early breeding stages but predicts no same-sex bias in response to male/female songs. Acoustic paternity-guarding predicts males will duet with mates during male playback and in their mate’s receptive stage, and they will bias aggression toward the speaker playing male song. Focal pairs duetted more during playback than controls and most during pre-breeding. Males and females responded more strongly to duet than solo playback, especially during pre-breeding, but neither showed same-sex response bias. Results most strongly supported the territory defense hypothesis, providing evidence that, despite cuckoldry risk, vocal duets were not used primarily for paternity-guarding. This helps us toward understanding the function of vocal displays across different mating systems.
    Print ISSN: 1045-2249
    Electronic ISSN: 1465-7279
    Topics: Biology
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  • 5
    Publication Date: 2016-12-01
    Description: Queuosine (Q) was discovered in the wobble position of a transfer RNA (tRNA) 47 years ago, yet the final biosynthetic enzyme responsible for Q-maturation, epoxyqueuosine (oQ) reductase (QueG), was only recently identified. QueG is a cobalamin (Cbl)-dependent, [4Fe-4S] cluster-containing protein that produces the hypermodified nucleoside Q in situ on four tRNAs. To understand how QueG is able to perform epoxide reduction, an unprecedented reaction for a Cbl-dependent enzyme, we have determined a series of high resolution structures of QueG from Bacillus subtilis . Our structure of QueG bound to a tRNA Tyr anticodon stem loop shows how this enzyme uses a HEAT-like domain to recognize the appropriate anticodons and position the hypermodified nucleoside into the enzyme active site. We find Q bound directly above the Cbl, consistent with a reaction mechanism that involves the formation of a covalent Cbl-tRNA intermediate. Using protein film electrochemistry, we show that two [4Fe-4S] clusters adjacent to the Cbl have redox potentials in the range expected for Cbl reduction, suggesting how Cbl can be activated for nucleophilic attack on oQ. Together, these structural and electrochemical data inform our understanding of Cbl dependent nucleic acid modification.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
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  • 6
    Publication Date: 2019-06-20
    Description: Several studies have linked mitochondrial genetic variation to phenotypic modifications; albeit the identity of the mitochondrial polymorphisms involved remains elusive. The search for these polymorphisms led to the discovery of small noncoding RNAs, which appear to be transcribed by the mitochondrial DNA (“small mitochondrial RNAs”). This contention is, however, controversial because the nuclear genome of most animals harbors mitochondrial pseudogenes (NUMTs) of identical sequence to regions of mtDNA, which could alternatively represent the source of these RNAs. To discern the likely contributions of the mitochondrial and nuclear genome to transcribing these small mitochondrial RNAs, we leverage data from six vertebrate species exhibiting markedly different levels of NUMT sequence. We explore whether abundances of small mitochondrial RNAs are associated with levels of NUMT sequence across species, or differences in tissue-specific mtDNA content within species. Evidence for the former would support the hypothesis these RNAs are primarily transcribed by NUMT sequence, whereas evidence for the latter would provide strong evidence for the counter hypothesis that these RNAs are transcribed directly by the mtDNA. No association exists between the abundance of small mitochondrial RNAs and NUMT levels across species. Moreover, a sizable proportion of transcripts map exclusively to the mtDNA sequence, even in species with highest NUMT levels. Conversely, tissue-specific abundances of small mitochondrial RNAs are strongly associated with the mtDNA content. These results support the hypothesis that small mitochondrial RNAs are primarily transcribed by the mitochondrial genome and that this capacity is conserved across Amniota and, most likely, across most metazoan lineages.
    Electronic ISSN: 1759-6653
    Topics: Biology
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  • 7
  • 8
    Publication Date: 2020-09-16
    Description: In addition to known genes, much of the human genome is transcribed into RNA. Chance formation of novel open reading frames (ORFs) can lead to the translation of myriad new proteins. Some of these ORFs may yield advantageous adaptive de novo proteins. However, widespread translation of non-coding DNA can also produce hazardous protein molecules, which can misfold andor form toxic aggregates. The dynamics of how de novo proteins emerge from potentially toxic raw materials and what influences their long-term survival are unknown. Here, using transcriptomic data from human and five other primates, we generate a set of transcribed human ORFs at six conservation levels to investigate which properties influence the early emergence and long-term retention of these expressed ORFs. As these taxa diverged from each other relatively recently we present a fine scale view of the evolution of novel sequences over recent evolutionary time. We find that novel human-restricted ORFs are preferentially located on GC-rich gene-dense chromosomes, suggesting their retention is linked to pre-existing genes. Sequence properties such as intrinsic structural disorder and aggregation propensity–which have been proposed to play a role in survival of de novo genes–remain relatively unchanged over time. Even very young sequences code for proteins with low aggregation propensities, suggesting that genomic regions with many novel transcribed ORFs are concomitantly less likely to produce ORFs which code for harmful toxic proteins. Our data indicate that the survival of these novel ORFs is largely stochastic rather than shaped by selection.
    Electronic ISSN: 1759-6653
    Topics: Biology
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  • 9
    Publication Date: 2020-05-22
    Description: The tremendous diversity of Hymenoptera is commonly attributed to the evolution of parasitoidism in the last common ancestor of parasitoid sawflies (Orussidae) and wasp-waisted Hymenoptera (Apocrita). However, Apocrita and Orussidae differ dramatically in their species richness, indicating that the diversification of Apocrita was promoted by additional traits. These traits have remained elusive due to a paucity of sawfly genome sequences, in particular those of parasitoid sawflies. Here, we present comparative analyses of draft genomes of the primarily phytophagous sawfly Athalia rosae and the parasitoid sawfly Orussus abietinus. Our analyses revealed that the ancestral hymenopteran genome exhibited traits that were previously considered unique to eusocial Apocrita (e.g., low transposable element content and activity) and a wider gene repertoire than previously thought (e.g., genes for CO2 detection). Moreover, we discovered that Apocrita evolved a significantly larger array of odorant receptors than sawflies, which could be relevant to the remarkable diversification of Apocrita by enabling efficient detection and reliable identification of hosts.
    Electronic ISSN: 1759-6653
    Topics: Biology
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  • 10
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