ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2012
Identification of E2F target genes that are rate limiting for dE2F1-dependent cell proliferation.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Normal cell cycle progression requires negative regulation of E2F1 by Groucho during S phase and its relief at G2 phase.Development (Cambridge, England) · 2023Article
- E2F regulation of theProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Large-scale gene co-expression network as a source of functional annotation for cattle genes.BMC genomics · 2016Article
- Discovery of progenitor cell signatures by time-series synexpression analysis during Drosophila embryonic cell immortalization.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundMicroarray studies have shown that the E2F transcription factor influences the expression of many genes but it is unclear how many of these targets are important for E2F-mediated control of cell proliferation.
resultsWe assembled a collection of mutant alleles of 44 dE2F1-dependent genes and tested whether these could modify visible phenotypes caused by the tissue-specific depletion of dE2F1. More than half of the mutant alleles dominantly enhanced de2f1-dsRNA phenotypes suggesting that the in vivo functions of dE2F1 can be limited by the reduction in the level of expression of many different targets. Unexpectedly, several mutant alleles suppressed de2f1-dsRNA phenotypes. One of the strongest of these suppressors was Orc5. Depletion of ORC5 increased proliferation in cells with reduced dE2F1 and specifically elevated the expression of dE2F1-regulated genes. Importantly, these effects were independent of dE2F1 protein levels, suggesting that reducing the level of ORC5 did not interfere with the general targeting of dE2F1.
conclusionsWe propose that the interaction between ORC5 and dE2F1 may reflect a feedback mechanism between replication initiation proteins and dE2F1 that ensures that proliferating cells maintain a robust level of replication proteins for the next cell cycle.
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