ArticlePLoS genetics2011
Caenorhabditis elegans cyclin D/CDK4 and cyclin E/CDK2 induce distinct cell cycle re-entry programs in differentiated muscle cells.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
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- MiR-24-3p Conservatively Regulates Muscle Cell Proliferation and Apoptosis by Targeting Common GeneAnimals : an open access journal from MDPI · 2022Article
- What programs the size of animal cells?Frontiers in cell and developmental biology · 2022Review
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- Identification of the critical replication targets of CDK reveals direct regulation of replication initiation factors by the embryo polarity machinery in C. elegans.PLoS genetics · 2020Article
- Changes in chromatin accessibility ensure robust cell cycle exit in terminally differentiated cells.PLoS biology · 2019Article
- Developmental Control of the Cell Cycle: Insights fromGenetics · 2019Review
- 6,7-Dihydroxy-2-(4'-hydroxyphenyl)naphthalene induces HCT116 cell apoptosis through activation of endoplasmic reticulum stress and the extrinsic apoptotic pathway.Drug design, development and therapy · 2019Article
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- Subunits of the DNA polymerase alpha-primase complex promote Notch-mediated proliferation with discrete and shared functions in C. elegans germline.The FEBS journal · 2018Article
- A population of G2-arrested cells are selected as sensory organ precursors for the interommatidial bristles of the Drosophila eye.Developmental biology · 2017Article
- Coordinating cell proliferation and differentiation: Antagonism between cell cycle regulators and cell type-specific gene expression.Cell cycle (Georgetown, Tex.) · 2016Review
- Early and Late G1/S Cyclins and Cdks Act Complementarily to Enhance Authentic Human β-Cell Proliferation and Expansion.Diabetes · 2015Article
- Scalloped and Yorkie are required for cell cycle re-entry of quiescent cells after tissue damage.Development (Cambridge, England) · 2015Article
- Rb and FZR1/Cdh1 determine CDK4/6-cyclin D requirement in C. elegans and human cancer cells.Nature communications · 2015Article
- Article
- Single molecule fluorescence approaches shed light on intracellular RNAs.Chemical reviews · 2014Review
- Signaling pathways that control cell proliferation.Cold Spring Harbor perspectives in biology · 2013Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell proliferation and differentiation are regulated in a highly coordinated and inverse manner during development and tissue homeostasis. Terminal differentiation usually coincides with cell cycle exit and is thought to engage stable transcriptional repression of cell cycle genes. Here, we examine the robustness of the post-mitotic state, using Caenorhabditis elegans muscle cells as a model. We found that expression of a G1 Cyclin and CDK initiates cell cycle re-entry in muscle cells without interfering with the differentiated state. Cyclin D/CDK4 (CYD-1/CDK-4) expression was sufficient to induce DNA synthesis in muscle cells, in contrast to Cyclin E/CDK2 (CYE-1/CDK-2), which triggered mitotic events. Tissue-specific gene-expression profiling and single molecule FISH experiments revealed that Cyclin D and E kinases activate an extensive and overlapping set of cell cycle genes in muscle, yet failed to induce some key activators of G1/S progression. Surprisingly, CYD-1/CDK-4 also induced an additional set of genes primarily associated with growth and metabolism, which were not activated by CYE-1/CDK-2. Moreover, CYD-1/CDK-4 expression also down-regulated a large number of genes enriched for catabolic functions. These results highlight distinct functions for the two G1 Cyclin/CDK complexes and reveal a previously unknown activity of Cyclin D/CDK-4 in regulating metabolic gene expression. Furthermore, our data demonstrate that many cell cycle genes can still be transcriptionally induced in post-mitotic muscle cells, while maintenance of the post-mitotic state might depend on stable repression of a limited number of critical cell cycle regulators.
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