ArticleDevelopmental biology2007
lin-35/Rb and the CoREST ortholog spr-1 coordinately regulate vulval morphogenesis and gonad development in C. elegans.
Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- HDAC1/2-mediated repression of Wnt receptor expression orients asymmetric division polarity in Caenorhabditis elegans.Development (Cambridge, England) · 2026Article
- Conserved chromatin regulators control the transcriptional immune response to intracellular pathogens in Caenorhabditis elegans.PLoS genetics · 2025Article
- The combination of metformin and high glucose increased longevity ofFrontiers in endocrinology · 2024Article
- Ketamine induces apical extracellular matrix modifications in Caenorhabditis elegans.Scientific reports · 2022Article
- Overlapping and non-overlapping roles of the class-I histone deacetylase-1 corepressors LET-418, SIN-3, and SPR-1 in Caenorhabditis elegans embryonic development.Genes & genomics · 2021Article
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- Integrity of Narrow Epithelial Tubes in the C. elegans Excretory System Requires a Transient Luminal Matrix.PLoS genetics · 2016Article
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- Evidence for autoregulation and cell signaling pathway regulation from genome-wide binding of the Drosophila retinoblastoma protein.G3 (Bethesda, Md.) · 2012Article
- A network of genes antagonistic to the LIN-35 retinoblastoma protein of Caenorhabditis elegans.Genetics · 2012Article
- mir-35 is involved in intestine cell G1/S transition and germ cell proliferation in C. elegans.Cell research · 2011Article
- Two Golgi-resident 3'-Phosphoadenosine 5'-phosphosulfate transporters play distinct roles in heparan sulfate modifications and embryonic and larval development in Caenorhabditis elegans.The Journal of biological chemistry · 2010Article
- Article
- Cancer models in Caenorhabditis elegans.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- A mechanistic basis for the coordinated regulation of pharyngeal morphogenesis in Caenorhabditis elegans by LIN-35/Rb and UBC-18-ARI-1.PLoS genetics · 2009Article
- Coordinated regulation of intestinal functions in C. elegans by LIN-35/Rb and SLR-2.PLoS genetics · 2008Article
- A suppressor screen in chlamydomonas identifies novel components of the retinoblastoma tumor suppressor pathway.Genetics · 2008Article
- The SynMuv genes of Caenorhabditis elegans in vulval development and beyond.Developmental biology · 2007Review
- Transcriptome profiling of the C. elegans Rb ortholog reveals diverse developmental roles.Developmental biology · 2007Article
- Morphogenesis of the caenorhabditis elegans vulva.Wiley interdisciplinary reviews. Developmental biologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Using a genetic screen to identify genes that carry out redundant functions during development with lin-35/Rb, the C. elegans Retinoblastoma family ortholog, we have identified a mutation in spr-1. spr-1 encodes the C. elegans ortholog of human CoREST, a protein containing Myb-like SANT and ELM2 domains, which functions as part of a transcriptional regulatory complex. CoREST recruits mediators of transcriptional repression, including histone deacetylase, and demethylase, and interacts with the tumor suppression protein REST. spr-1/CoREST was previously shown in C. elegans to suppress defects associated with loss of the presenilin sel-12, which functions in the proteolytic processing of LIN-12/Notch. Here we show that lin-35 and spr-1 coordinately regulate several developmental processes in C. elegans including the ingression of vulval cells as well as germline proliferation. We also show that loss of lin-35 and spr-1 hypersensitizes animals to a reduction in LIN-12/Notch activity, leading to the generation of proximal germline tumors. This defect, which is observed in lin-35; spr-1; lin-12(RNAi) and lin-35; spr-1; hop-1(RNAi) triple mutants is likely due to a delay in the entry of germ cells into meiosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.