Blimp1 defines a progenitor population that governs cellular input to the sebaceous gland

被引:342
作者
Horsley, Valerie
O'Carroll, Donal
Tooze, Reuben
Ohinata, Yasuhide
Saitou, Mitinori
Obukhanych, Tetyana
Nussenzweig, Michel
Tarakhovsky, Alexander
Fuchs, Elaine [1 ]
机构
[1] Rockefeller Univ, Howard Hughes Med Inst, Lab Mammalian Cell Biol & Dev, New York, NY 10021 USA
[2] Rockefeller Univ, Howard Hughes Med Inst, Lab Lymphocyte Signaling, New York, NY 10021 USA
[3] Rockefeller Univ, Howard Hughes Med Inst, Lab Mol Immunol, New York, NY 10021 USA
[4] Univ Leeds, Leeds Inst Mol Med, Div Expt Haematol, Leeds LS9 7TF, W Yorkshire, England
[5] RIKEN, Kobe Inst, Ctr Dev Biol, Lab Mammalian Germ Cell Biol,Chuo Ku, Kobe, Hyogo 6500047, Japan
基金
英国医学研究理事会;
关键词
D O I
10.1016/j.cell.2006.06.048
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epidermal lineage commitment occurs when multipotent stem cells are specified to three lineages: the epidermis, the hair follicle, and the sebaceous gland (SG). How and when a lineage becomes specified remains unknown. Here, we report the existence of a population of unipotent progenitor cells that reside in the SG and express the transcriptional repressor Blimp1. Using cell-culture studies and genetic lineage tracing, we demonstrate that Blimp1-expressing cells are upstream from other cells of the SG lineage. Blimp1 appears to govern cellular input into the gland since its loss leads to elevated c-myc expression, augmented cell proliferation, and SG hyperplasia. Finally, BrdU labeling experiments demonstrate that the SG defects associated with loss of Blimp1 lead to enhanced bulge stem cell activity, suggesting that when normal SG homeostasis is perturbed, multipotent stem cells in the bulge can be mobilized to correct this imbalance.
引用
收藏
页码:597 / 609
页数:13
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