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Stem/progenitor cells coordinate proliferation and differentiation, giving rise to appropriate cell numbers of functionally specialized cells during organogenesis. In different experimental systems, Geminin was shown to maintain progenitor cells and participate in fate determination decisions and organogenesis. Although the exact mechanisms are unclear, Geminin has been postulated to influence proliferation versus differentiation decisions. To gain insight into the in vivo role of Geminin in progenitor cell division and differentiation, we have generated mice that specifically lack Geminin in cells of lymphoid lineage through Cre-mediated recombination. T cells lacking Geminin expression upregulate early activation markers efficiently upon TCR stimulation in vitro and are able to enter the S phase of cell cycle, but show a marked defect in completing the cycle, leading to a large proportion of T cells accumulating in S/G2/M phases. Accordingly, T cells deficient in Geminin show a reduced ability to repopulate lymphopenic hosts in vivo. Contrary to expectations, Geminin deficiency does not alter development and differentiation of T cells in vivo. Our data suggest that Geminin is required for the proliferation events taking place either in vitro upon TCR receptor activation or during homeostatic expansion, but appears to be redundant for the proliferation and differentiation of the majority of progenitor T cell populations.

Original publication

DOI

10.4049/jimmunol.0901983

Type

Journal article

Journal

J Immunol

Publication Date

01/03/2010

Volume

184

Pages

2432 - 2441

Keywords

Animals, Blotting, Western, Cell Cycle, Cell Cycle Proteins, Cell Division, Cell Lineage, Cell Proliferation, Cells, Cultured, DNA-Binding Proteins, Flow Cytometry, G2 Phase, Geminin, Homeostasis, Lymphoid Tissue, Mice, Mice, Inbred C57BL, Mice, Knockout, Nuclear Proteins, S Phase, Spleen, T-Lymphocytes, Thymus Gland