ArticleCell cycle (Georgetown, Tex.)2009
The cyclin-dependent kinase inhibitors, cki-1 and cki-2, act in overlapping but distinct pathways to control cell cycle quiescence during C. elegans development.
Article in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed.
- Quantification ofmicroPublication biology · 2026Article
- Unusual inheritance of a functionalScience advances · 2025Article
- CDK-4 regulates nucleolar size and metabolism at the cost of late-life fitness in C. elegans.Heredity · 2025Article
- Robustness and variability inbioRxiv : the preprint server for biology · 2024Article
- COP9 signalosome component CSN-5 stabilizes PUF proteins FBF-1 and FBF-2 in Caenorhabditis elegans germline stem and progenitor cells.Genetics · 2024Article
- Cell cycle perturbation uncouples mitotic progression and invasive behavior in a post-mitotic cell.bioRxiv : the preprint server for biology · 2024Article
- Targeted DamID inScience advances · 2022Article
- Negative feedback by conserved kinases patterns the degradation ofDevelopment (Cambridge, England) · 2020Article
- Diverse Roles of PUF Proteins in Germline Stem and Progenitor Cell Development inFrontiers in cell and developmental biology · 2020Review
- Developmental Control of the Cell Cycle: Insights fromGenetics · 2019Review
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- LIN-41 inactivation leads to delayed centrosome elimination and abnormal chromosome behavior during female meiosis in Caenorhabditis elegans.Molecular biology of the cell · 2016Article
- Identification of Wnt Pathway Target Genes Regulating the Division and Differentiation of Larval Seam Cells and Vulval Precursor Cells in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2015Article
- A model of the regulatory network involved in the control of the cell cycle and cell differentiation in the Caenorhabditis elegans vulva.BMC bioinformatics · 2015Article
- The C. elegans NR4A nuclear receptor gene nhr-6 promotes cell cycle progression in the spermatheca lineage.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- A complex regulatory network coordinating cell cycles during C. elegans development is revealed by a genome-wide RNAi screen.G3 (Bethesda, Md.) · 2014Article
- Stem cell proliferation versus meiotic fate decision in Caenorhabditis elegans.Advances in experimental medicine and biology · 2013Review
- Control of oocyte growth and meiotic maturation in Caenorhabditis elegans.Advances in experimental medicine and biology · 2013Review
- Analysis of centriole elimination during C. elegans oogenesis.Development (Cambridge, England) · 2012Article
- A novel mutation in β integrin reveals an integrin-mediated interaction between the extracellular matrix and cki-1/p27KIP1.PloS one · 2012Article
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Abstract
Cyclin-dependent kinase inhibitors (CKIs) are major contributors to the decision to enter or exit the cell cycle. The Caenorhabditis elegans genome encodes two CKIs belonging to the Cip/Kip family, cki-1 and cki-2. cki-1 has been shown to act as a canonical negative regulator of cell cycle entry, while the role of cki-2 remains unclear. We identified cki-2 in a genome-wide RNAi screen to reveal genes essential for developmental cell cycle quiescence. Examination of cki-2 knockout animals revealed extra rounds of cell divisions, verifying a role in establishing or maintaining the temporary cell cycle arrest. Despite the overlapping defects, the pathways mediated by cki-1 and cki-2 are discrete since the extra cell phenotype conferred by a putative cki-2(null) mutation is enhanced upon additional loss of cki-1 activity. Moreover, the extra cell division defect of cki-2 is not increased with the additional loss of lin-35 Rb, as is seen with cki-1. Thus, both cki-1 and cki-2 mediate cell cycle quiescence, but our genetic and phenotypic analyses demonstrate that they act within distinct pathways to exert control over the cell cycle machinery.
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