Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice

The Polycomb group (PcG) gene Bmi1 promotes cell proliferation and stem cell self-renewal by repressing the Ink4a/Arf locus. We used a genetic approach to investigate whether Ink4a or Arf is more critical for relaying Bmi1 function in lymphoid cells, neural progenitors, and neural stem cells. We sho...

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Vydané v:Genes & development Ročník 19; číslo 12; s. 1438
Hlavní autori: Bruggeman, Sophia W M, Valk-Lingbeek, Merel E, van der Stoop, Petra P M, Jacobs, Jacqueline J L, Kieboom, Karin, Tanger, Ellen, Hulsman, Danielle, Leung, Carly, Arsenijevic, Yvan, Marino, Silvia, van Lohuizen, Maarten
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 15.06.2005
Predmet:
Animals
Cell Differentiation
Cell Proliferation
Cellular Senescence
Cerebellum - cytology
Cyclin-Dependent Kinase Inhibitor p16 - deficiency
Cyclin-Dependent Kinase Inhibitor p16 - metabolism
Genes, p16
Heterozygote
Lymphoid Tissue - cytology
Mice
Mice, Inbred C57BL
Mice, Knockout
Multipotent Stem Cells - cytology
Multipotent Stem Cells - metabolism
Neurons - cytology
Neurons - metabolism
Nuclear Proteins - deficiency
Nuclear Proteins - genetics
Polycomb Repressive Complex 1
Proto-Oncogene Proteins - deficiency
Proto-Oncogene Proteins - genetics
Repressor Proteins - genetics
Repressor Proteins - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Tumor Suppressor Protein p14ARF - deficiency
Tumor Suppressor Protein p14ARF - genetics
Tumor Suppressor Protein p14ARF - metabolism
ISSN:0890-9369
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Popis
Shrnutí:The Polycomb group (PcG) gene Bmi1 promotes cell proliferation and stem cell self-renewal by repressing the Ink4a/Arf locus. We used a genetic approach to investigate whether Ink4a or Arf is more critical for relaying Bmi1 function in lymphoid cells, neural progenitors, and neural stem cells. We show that Arf is a general target of Bmi1, however particularly in neural stem cells, derepression of Ink4a contributes to Bmi1(-/-) phenotypes. Additionally, we demonstrate haploinsufficient effects for the Ink4a/Arf locus downstream of Bmi1 in vivo. This suggests differential, cell type-specific roles for Ink4a versus Arf in PcG-mediated (stem) cell cycle control.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0890-9369
DOI:10.1101/gad.1299305