Abstract
The interplay of proliferation and differentiation is essential for normal development and organogenesis. Geminin is a cell cycle regulator which controls licensing of origins for DNA replication, safeguarding genomic stability. Geminin has also been shown to regulate cellular decisions of self-renewal versus commitment of neuronal progenitor cells. We discuss here our recent analysis of mice with conditional inactivation of the Geminin gene in the immune system. Our data indicate that Geminin is not indispensable for every cell division: in the absence of Geminin, development of progenitor T cells appears largely unaffected. In contrast, rapid cell divisions, taking place in vitro upon TCR receptor activation or in vivo during homeostatic proliferation, are defective.
MeSH terms
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Animals
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism*
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Cell Cycle Proteins / physiology
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Cell Differentiation
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Cell Proliferation
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Chromosomal Proteins, Non-Histone / metabolism
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DNA Replication
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DNA-Binding Proteins / metabolism
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G1 Phase
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Geminin
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Genomic Instability
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Mice
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism*
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Nuclear Proteins / physiology
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Polycomb-Group Proteins
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Repressor Proteins / metabolism
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism
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Transcription Factors / metabolism
Substances
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Cell Cycle Proteins
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Chromosomal Proteins, Non-Histone
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DNA-Binding Proteins
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Geminin
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Gmnn protein, mouse
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Nuclear Proteins
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Polycomb-Group Proteins
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Repressor Proteins
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Ris2 protein, mouse
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SWI-SNF-B chromatin-remodeling complex
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Transcription Factors