ALBERT

Description: There are fundamental similarities between sleep in mammals and quiescence in the arthropod Drosophila melanogaster, suggesting that sleep-like states are evolutionarily ancient. The nematode Caenorhabditis elegans also has a quiescent behavioural state during a period called lethargus, which occurs before each of the four moults. Like sleep, lethargus maintains a constant temporal relationship with the expression of the C. elegans Period homologue LIN-42 (ref. 5). Here we show that quiescence associated with lethargus has the additional sleep-like properties of reversibility, reduced responsiveness and homeostasis. We identify the cGMP-dependent protein kinase (PKG) gene egl-4 as a regulator of sleep-like behaviour, and show that egl-4 functions in sensory neurons to promote the C. elegans sleep-like state. Conserved effects on sleep-like behaviour of homologous genes in C. elegans and Drosophila suggest a common genetic regulation of sleep-like states in arthropods and nematodes. Our results indicate that C. elegans is a suitable model system for the study of sleep regulation. The association of this C. elegans sleep-like state with developmental changes that occur with larval moults suggests that sleep may have evolved to allow for developmental changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raizen, David M -- Zimmerman, John E -- Maycock, Matthew H -- Ta, Uyen D -- You, Young-jai -- Sundaram, Meera V -- Pack, Allan I -- England -- Nature. 2008 Jan 31;451(7178):569-72. doi: 10.1038/nature06535. Epub 2008 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Sleep and Respiratory Neurobiology, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, Pennsylvania 19104, USA. raizen@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18185515" target="_blank"〉PubMed〈/a〉

Description: To broaden our understanding of the evolution of gene regulation mechanisms, we generated occupancy profiles for 34 orthologous transcription factors (TFs) in human-mouse erythroid progenitor, lymphoblast and embryonic stem-cell lines. By combining the genome-wide transcription factor occupancy repertoires, associated epigenetic signals, and co-association patterns, here we deduce several evolutionary principles of gene regulatory features operating since the mouse and human lineages diverged. The genomic distribution profiles, primary binding motifs, chromatin states, and DNA methylation preferences are well conserved for TF-occupied sequences. However, the extent to which orthologous DNA segments are bound by orthologous TFs varies both among TFs and with genomic location: binding at promoters is more highly conserved than binding at distal elements. Notably, occupancy-conserved TF-occupied sequences tend to be pleiotropic; they function in several tissues and also co-associate with many TFs. Single nucleotide variants at sites with potential regulatory functions are enriched in occupancy-conserved TF-occupied sequences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4343047/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4343047/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Yong -- Ma, Zhihai -- Kim, Bong-Hyun -- Wu, Weisheng -- Cayting, Philip -- Boyle, Alan P -- Sundaram, Vasavi -- Xing, Xiaoyun -- Dogan, Nergiz -- Li, Jingjing -- Euskirchen, Ghia -- Lin, Shin -- Lin, Yiing -- Visel, Axel -- Kawli, Trupti -- Yang, Xinqiong -- Patacsil, Dorrelyn -- Keller, Cheryl A -- Giardine, Belinda -- Mouse ENCODE Consortium -- Kundaje, Anshul -- Wang, Ting -- Pennacchio, Len A -- Weng, Zhiping -- Hardison, Ross C -- Snyder, Michael P -- 1U54HG00699/HG/NHGRI NIH HHS/ -- 3RC2HG005602/HG/NHGRI NIH HHS/ -- 5U54HG006996/HG/NHGRI NIH HHS/ -- R01 DK065806/DK/NIDDK NIH HHS/ -- R01 DK096266/DK/NIDDK NIH HHS/ -- R01 ES024992/ES/NIEHS NIH HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R01 GM083337/GM/NIGMS NIH HHS/ -- R01 HG003988/HG/NHGRI NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG007175/HG/NHGRI NIH HHS/ -- R01 HG007348/HG/NHGRI NIH HHS/ -- R01 HG007354/HG/NHGRI NIH HHS/ -- R01DK065806/DK/NIDDK NIH HHS/ -- R01HG003988/HG/NHGRI NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- RC2 HG005573/HG/NHGRI NIH HHS/ -- RC2 HG005602/HG/NHGRI NIH HHS/ -- RC2HG005573/HG/NHGRI NIH HHS/ -- U01 DE024427/DE/NIDCR NIH HHS/ -- U41 HG007234/HG/NHGRI NIH HHS/ -- U54 HG006996/HG/NHGRI NIH HHS/ -- U54 HG006997/HG/NHGRI NIH HHS/ -- U54 HG006998/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- U54HG006997/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Nov 20;515(7527):371-5. doi: 10.1038/nature13985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University, Stanford, California 94305, USA. ; Program in Bioinformatics and Integrative Biology, Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; 1] Center for Comparative Genomics and Bioinformatics, Huck Institutes of the Life Sciences, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA [2] BRCF Bioinformatics Core, University of Michigan, Ann Arbor, Michigan 48105, USA. ; Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St Louis, Missouri 63108, USA. ; Center for Comparative Genomics and Bioinformatics, Huck Institutes of the Life Sciences, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; 1] Department of Genetics, Stanford University, Stanford, California 94305, USA [2] Division of Cardiovascular Medicine, Stanford University, Stanford, California 94304, USA. ; 1] Department of Genetics, Stanford University, Stanford, California 94305, USA [2] Department of Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; 1] Lawrence Berkeley National Laboratory, Genomics Division, Berkeley, California 94701, USA [2] Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA [3] School of Natural Sciences, University of California, Merced, California 95343, USA. ; 1] Lawrence Berkeley National Laboratory, Genomics Division, Berkeley, California 94701, USA [2] Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409826" target="_blank"〉PubMed〈/a〉

Description: The AFF-1 exoplasmic fusogen is required for endocytic scission and seamless tube elongation The AFF-1 exoplasmic fusogen is required for endocytic scission and seamless tube elongation, Published online: 01 May 2018; doi:10.1038/s41467-018-04091-1 Membrane fusion and fission events at exoplasmic membrane surfaces are not well understood. Here the authors show that the C. elegans cell–cell fusogen AFF-1 is required for endocytic scission and apically-directed membrane trafficking during the development of a unicellular tube.