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E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells
Nature (London), 2009-12, Vol.462 (7275), p.930-934
2009
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Autor(en) / Beteiligte
Titel
E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells
Ist Teil von
  • Nature (London), 2009-12, Vol.462 (7275), p.930-934
Ort / Verlag
London: Nature Publishing Group
Erscheinungsjahr
2009
Quelle
MEDLINE
Beschreibungen/Notizen
  • In the established model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells from entering S phase by binding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ultimate effectors of a transcriptional program that commit cells to enter and progress through S phase. Using a panel of tissue-specific cre-transgenic mice and conditional E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem cells, embryos and small intestines. We show that in normal dividing progenitor cells E2f1-3 function as transcriptional activators, but contrary to the current view, are dispensable for cell division and instead are necessary for cell survival. In differentiating cells E2f1-3 function in a complex with Rb as repressors to silence E2f targets and facilitate exit from the cell cycle. The inactivation of Rb in differentiating cells resulted in a switch of E2f1-3 from repressors to activators, leading to the superactivation of E2f responsive targets and ectopic cell divisions. Loss of E2f1-3 completely suppressed these phenotypes caused by Rb deficiency. This work contextualizes the activator versus repressor functions of E2f1-3 in vivo, revealing distinct roles in dividing versus differentiating cells and in normal versus cancer-like cell cycles.
Sprache
Englisch
Identifikatoren
ISSN: 0028-0836
eISSN: 1476-4687
DOI: 10.1038/nature08677
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2806193
Format
–
Schlagworte
Alleles, Animals, Apoptosis, Biological and medical sciences, Cell cycle, Cell Cycle - genetics, Cell Cycle - physiology, Cell Differentiation, Cell division, Cell Proliferation, E2F Transcription Factors - deficiency, E2F Transcription Factors - genetics, E2F Transcription Factors - metabolism, E2F1 Transcription Factor - deficiency, E2F1 Transcription Factor - genetics, E2F1 Transcription Factor - metabolism, E2F2 Transcription Factor - deficiency, E2F2 Transcription Factor - genetics, E2F2 Transcription Factor - metabolism, E2F3 Transcription Factor - deficiency, E2F3 Transcription Factor - genetics, E2F3 Transcription Factor - metabolism, Embryo, Mammalian - cytology, Embryo, Mammalian - metabolism, Embryonic stem cells, Embryonic Stem Cells - cytology, Embryonic Stem Cells - metabolism, Female, Fundamental and applied biological sciences. Psychology, Gene expression, Gene Expression Regulation, General aspects (metabolism, cell proliferation, established cell line...), Genetic aspects, Independent sample, Intestine, Small - cytology, Intestine, Small - metabolism, Intestine. Mesentery, Medical sciences, Mice, Mice, Transgenic, Physiological aspects, Repressor Proteins - deficiency, Repressor Proteins - genetics, Repressor Proteins - metabolism, Retinoblastoma Protein - deficiency, Retinoblastoma Protein - metabolism, Rodents, Stem cells, Transcription factors, Tumor cell, Tumors, Vertebrates: digestive system

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