| Literature DB >> 28041896 |
Shang Cai1, Tomer Kalisky2, Debashis Sahoo3, Piero Dalerba4, Weiguo Feng5, Yuan Lin5, Dalong Qian1, Angela Kong1, Jeffrey Yu1, Flora Wang1, Elizabeth Y Chen1, Ferenc A Scheeren1, Angera H Kuo1, Shaheen S Sikandar1, Shigeo Hisamori1, Linda J van Weele1, Diane Heiser1, Sopheak Sim1, Jessica Lam1, Stephen Quake2, Michael F Clarke6.
Abstract
Stem cells in many tissues sustain themselves by entering a quiescent state to avoid genomic insults and to prevent exhaustion caused by excessive proliferation. In the mammary gland, the identity and characteristics of quiescent epithelial stem cells are not clear. Here, we identify a quiescent mammary epithelial cell population expressing high levels of Bcl11b and located at the interface between luminal and basal cells. Bcl11bhigh cells are enriched for cells that can regenerate mammary glands in secondary transplants. Loss of Bcl11b leads to a Cdkn2a-dependent exhaustion of ductal epithelium and loss of epithelial cell regenerative capacity. Gain- and loss-of-function studies show that Bcl11b induces cells to enter the G0 phase of the cell cycle and become quiescent. Taken together, these results suggest that Bcl11b acts as a central intrinsic regulator of mammary epithelial stem cell quiescence and exhaustion and is necessary for long-term maintenance of the mammary gland.Entities:
Keywords: quiescence; stem cell exhaustion
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Year: 2016 PMID： 28041896 PMCID： PMC5341693 DOI： 10.1016/j.stem.2016.11.007
Source DB: PubMed Journal: Cell Stem Cell ISSN： 1875-9777 Impact factor: 24.633