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Jarid2 调控小鼠表皮干细胞的激活和分化。

Jarid2 regulates mouse epidermal stem cell activation and differentiation.

机构信息

Department of Differentiation and Cancer, Center for Genomic Regulation and UPF, Barcelona, Spain.

出版信息

EMBO J. 2011 Aug 2;30(17):3635-46. doi: 10.1038/emboj.2011.265.

Abstract

Jarid2 is required for the genomic recruitment of the polycomb repressive complex-2 (PRC2) in embryonic stem cells. However, its specific role during late development and adult tissues remains largely uncharacterized. Here, we show that deletion of Jarid2 in mouse epidermis reduces the proliferation and potentiates the differentiation of postnatal epidermal progenitors, without affecting epidermal development. In neonatal epidermis, Jarid2 deficiency reduces H3K27 trimethylation, a chromatin repressive mark, in epidermal differentiation genes previously shown to be targets of the PRC2. However, in adult epidermis Jarid2 depletion does not affect interfollicular epidermal differentiation but results in delayed hair follicle (HF) cycling as a consequence of decreased proliferation of HF stem cells and their progeny. We conclude that Jarid2 is required for the scheduled proliferation of epidermal stem and progenitor cells necessary to maintain epidermal homeostasis.

摘要

Jarid2 对于多梳抑制复合物 2(PRC2)在胚胎干细胞中的基因组募集是必需的。然而,其在后期发育和成人组织中的具体作用在很大程度上仍未被描述。在这里,我们表明,在小鼠表皮中删除 Jarid2 会减少出生后表皮祖细胞的增殖并促进其分化,而不会影响表皮发育。在新生表皮中,Jarid2 缺乏会降低先前被证明是 PRC2 靶标的表皮分化基因的 H3K27 三甲基化,这是一种染色质抑制标记。然而,在成年表皮中,Jarid2 耗竭并不影响毛囊间表皮的分化,但会导致毛囊(HF)循环延迟,这是由于 HF 干细胞及其后代增殖减少所致。我们得出结论,Jarid2 对于维持表皮内稳态所需的表皮干细胞和祖细胞的有计划增殖是必需的。

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