WormBase 2012: more genomes, more data, new website

Yook, Karen; Harris, Todd W.; Bieri, Tamberlyn; Cabunoc, Abigail; Chan, Juancarlos; Chen, Wen J.; Davis, Paul A.; Cruz, Norie De La; Duong, Adrian; Fang, Ruihua; Ganesan, Uma; Grove, Christian A.; Howe, Kevin; Kadam, Snehalata; Kishore, Ranjana; Lee, Raymond Y. N.; Li, Yuling; Müller, Hans‐Michael; Nakamura, Cecilia; Nash, Bill; Ozersky, Philip; Paulini, Michael; Raciti, Daniela; Rangarajan, Arun; Schindelman, Gary; Shi, Xiaoqi; Schwarz, Erich M.; Tuli, Mary Ann; Auken, Kimberly Van; Wang, Daniel; Wang, Xiaodong; Williams, Gary W.; Hodgkin, Jonathan; Berriman, Matthew; Durbin, Richard; Kersey, Paul J.; Strouboulis, John; Stein, Lincoln; Sternberg, Paul W.

doi:10.1093/nar/gkr954

Cited by 173 publications

(196 citation statements)

References 37 publications

(39 reference statements)

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“…gff2, downloaded from WormBase (Yook et al 2012), which annotates 2390 repeat elements in the studied region. Repeats are classed into 594 categories, which include several types of simple sequence repeats and low-complexity tracts (e.g., TTTA n , polypyrimadine, A rich, etc.…”

Section: Annotation Analysismentioning

confidence: 99%

Crossover Heterogeneity in the Absence of Hotspots inCaenorhabditis elegans

Kaur

Rockman

2014

Genetics

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Crossovers play mechanical roles in meiotic chromosome segregation, generate genetic diversity by producing new allelic combinations, and facilitate evolution by decoupling linked alleles. In almost every species studied to date, crossover distributions are dramatically nonuniform, differing among sexes and across genomes, with spatial variation in crossover rates on scales from whole chromosomes to subkilobase hotspots. To understand the regulatory forces dictating these heterogeneous distributions a crucial first step is the fine-scale characterization of crossover distributions. Here we define the wild-type distribution of crossovers along a region of the C. elegans chromosome II at unprecedented resolution, using recombinant chromosomes of 243 hermaphrodites and 226 males. We find that well-characterized large-scale domains, with little fine-scale rate heterogeneity, dominate this region's crossover landscape. Using the Gini coefficient as a summary statistic, we find that this region of the C. elegans genome has the least heterogeneous fine-scale crossover distribution yet observed among model organisms, and we show by simulation that the data are incompatible with a mammalian-type hotspot-rich landscape. The large-scale structural domains-the low-recombination center and the high-recombination arm-have a discrete boundary that we localize to a small region. This boundary coincides with the armcenter boundary defined both by nuclear-envelope attachment of DNA in somatic cells and GC content, consistent with proposals that these features of chromosome organization may be mechanical causes and evolutionary consequences of crossover recombination. MEIOTIC recombination creates novel combinations of parental alleles and is a powerful force shaping the genetic variation observed within a population. The frequency of recombination has a profound impact on the efficacy of natural selection in both purging deleterious mutations and in the formation of beneficial allelic combinations (Hill and Robertson 1966;Cutter and Payseur 2013). However, the intensity of recombination in different parts of a genome is rarely constant. Heterogeneity in the meiotic recombination rate has been observed across chromosome lengths and at finer scales of a few kilobase in diverse organisms.In Caenorhabditis elegans, meiotic recombination rates show a striking and reproducible chromosome-wide pattern of variation. Genetic maps of the five autosomes and X chromosome show that each has a low-recombination central domain flanked by high-recombination arm domains (Barnes et al. 1995;Rockman and Kruglyak 2009). This domain structure has dramatic effects on genetic variation and evolution (Cutter and Payseur 2003;Rockman et al. 2010;Andersen et al. 2012), but the underlying causes generating this pattern are not completely understood.The domain structure relates to unusual characteristics of the C. elegans chromosomes. The chromosomes lack localized centromeres and exhibit holocentric segregation during mitosis, with kinetochore pro...

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Section: Annotation Analysismentioning

confidence: 99%

Crossover Heterogeneity in the Absence of Hotspots inCaenorhabditis elegans

Kaur

Rockman

2014

Genetics

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“…Orthologs of C. elegans genes were identified using either the Homologene database at the National Center for Biotechnology Information or the Panther database from within WormBase (Mi et al 2010;Sayers et al 2012;Yook et al 2012). RNAi was performed largely as described previously (Alper et al 2008).…”

Section: Use Of Rnai In Mouse Macrophages To Test Candidate Genesmentioning

confidence: 99%

Comparative Genomics RNAi Screen Identifies Eftud2 as a Novel Regulator of Innate Immunity

et al. 2014

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The extent of the innate immune response is regulated by many positively and negatively acting signaling proteins. This allows for proper activation of innate immunity to fight infection while ensuring that the response is limited to prevent unwanted complications. Thus mutations in innate immune regulators can lead to immune dysfunction or to inflammatory diseases such as arthritis or atherosclerosis. To identify novel innate immune regulators that could affect infectious or inflammatory disease, we have taken a comparative genomics RNAi screening approach in which we inhibit orthologous genes in the nematode Caenorhabditis elegans and murine macrophages, expecting that genes with evolutionarily conserved function also will regulate innate immunity in humans. Here we report the results of an RNAi screen of approximately half of the C. elegans genome, which led to the identification of many candidate genes that regulate innate immunity in C. elegans and mouse macrophages. One of these novel conserved regulators of innate immunity is the mRNA splicing regulator Eftud2, which we show controls the alternate splicing of the MyD88 innate immunity signaling adaptor to modulate the extent of the innate immune response.

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“…Experiments were performed at 20°C unless noted. The genes and alleles in this work are described in Wormbase (www.wormbase.org) (Harris et al, 2010;Yook et al, 2012) unless otherwise indicated.…”

Section: Strains and Allelesmentioning

confidence: 99%

C. elegansGATA factors EGL-18 and ELT-6 function downstream of Wnt signaling to maintain the progenitor fate during larval asymmetric divisions of the seam cells

2013

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SUMMARYThe C. elegans seam cells are lateral epithelial cells arrayed in a single line from anterior to posterior that divide in an asymmetric, stem cell-like manner during larval development. These asymmetric divisions are regulated by Wnt signaling; in most divisions, the posterior daughter in which the Wnt pathway is activated maintains the progenitor seam fate, while the anterior daughter in which the Wnt pathway is not activated adopts a differentiated hypodermal fate. Using mRNA tagging and microarray analysis, we identified the functionally redundant GATA factor genes egl-18 and elt-6 as Wnt pathway targets in the larval seam cells. EGL-18 and ELT-6 have previously been shown to be required for initial seam cell specification in the embryo. We show that in larval seam cell asymmetric divisions, EGL-18 is expressed strongly in the posterior seam-fated daughter. egl-18 and elt-6 are necessary for larval seam cell specification, and for hypodermal to seam cell fate transformations induced by ectopic Wnt pathway overactivation. The TCF homolog POP-1 binds a site in the egl-18 promoter in vitro, and this site is necessary for robust seam cell expression in vivo. Finally, larval overexpression of EGL-18 is sufficient to drive expression of a seam marker in other hypodermal cells in wild-type animals, and in anterior hypodermal-fated daughters in a Wnt pathway-sensitized background. These data suggest that two GATA factors that are required for seam cell specification in the embryo independently of Wnt signaling are reused downstream of Wnt signaling to maintain the progenitor fate during stem cell-like divisions in larval development. KEY WORDS: C. elegans, Wnt signaling, Asymmetric cell divisionC. elegans GATA factors EGL-18 and ELT-6 function downstream of Wnt signaling to maintain the progenitor fate during larval asymmetric divisions of the seam cells

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WormBase 2012: more genomes, more data, new website

Cited by 173 publications

References 37 publications

Crossover Heterogeneity in the Absence of Hotspots inCaenorhabditis elegans

Crossover Heterogeneity in the Absence of Hotspots inCaenorhabditis elegans

Comparative Genomics RNAi Screen Identifies Eftud2 as a Novel Regulator of Innate Immunity

C. elegansGATA factors EGL-18 and ELT-6 function downstream of Wnt signaling to maintain the progenitor fate during larval asymmetric divisions of the seam cells

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