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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6961
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pubmed:dateCreated |
2003-10-30
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pubmed:abstractText |
Stem cells persist throughout life by self-renewing in numerous tissues including the central and peripheral nervous systems. This raises the issue of whether there is a conserved mechanism to effect self-renewing divisions. Deficiency in the polycomb family transcriptional repressor Bmi-1 leads to progressive postnatal growth retardation and neurological defects. Here we show that Bmi-1 is required for the self-renewal of stem cells in the peripheral and central nervous systems but not for their survival or differentiation. The reduced self-renewal of Bmi-1-deficient neural stem cells leads to their postnatal depletion. In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation. p16Ink4a deficiency partially reverses the self-renewal defect in Bmi-1-/- neural stem cells. This conserved requirement for Bmi-1 to promote self-renewal and to repress p16Ink4a expression suggests that a common mechanism regulates the self-renewal and postnatal persistence of diverse types of stem cell. Restricted neural progenitors from the gut and forebrain proliferate normally in the absence of Bmi-1. Thus, Bmi-1 dependence distinguishes stem cell self-renewal from restricted progenitor proliferation in these tissues.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-10089888,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-10710306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-11062467,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-11507641,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-11544531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12020801,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12194865,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12194866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12372282,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12482990,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12573439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12714970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-12714971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7715727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7867073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7906858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7910115,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7926765,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-7969470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-8414519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-8446631,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-8616889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-8887324,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-9244355,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-9285685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-9584124,
http://linkedlifedata.com/resource/pubmed/commentcorrection/14574365-9923679
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1476-4687
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
425
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
962-7
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pubmed:dateRevised |
2010-12-3
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pubmed:meshHeading |
pubmed-meshheading:14574365-Animals,
pubmed-meshheading:14574365-Apoptosis,
pubmed-meshheading:14574365-Cell Differentiation,
pubmed-meshheading:14574365-Cell Division,
pubmed-meshheading:14574365-Cell Lineage,
pubmed-meshheading:14574365-Cell Survival,
pubmed-meshheading:14574365-Cyclin-Dependent Kinase Inhibitor p16,
pubmed-meshheading:14574365-Mice,
pubmed-meshheading:14574365-Mice, Inbred C57BL,
pubmed-meshheading:14574365-Nervous System,
pubmed-meshheading:14574365-Neural Crest,
pubmed-meshheading:14574365-Neurons,
pubmed-meshheading:14574365-Nuclear Proteins,
pubmed-meshheading:14574365-Proto-Oncogene Proteins,
pubmed-meshheading:14574365-Repressor Proteins,
pubmed-meshheading:14574365-Stem Cells
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pubmed:year |
2003
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pubmed:articleTitle |
Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation.
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pubmed:affiliation |
Howard Hughes Medical Institute, and Departments of Internal Medicine and Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109-0934, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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