期刊
CELL REPORTS
卷 21, 期 8, 页码 2160-2170出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.10.091
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资金
- National Basic Research Program of China [2014CB965200]
- National Key R&D Program of China [2017YFJC040188, 2016YFA0101800, 2016YFA0100400]
- National Natural Science Foundation of China [31771424, 31522033, 31421004, 91419310, 31401084, 31501185, 31530038]
- Frontier Science Research Program'' of the CAS [QYZDJ-SSW-SMC009]
- Strategic Priority Research Program'' of the CAS [XDA01020401]
- Science and Technology Planning Project of Guangdong Province [2014B020225002, 2015B020228003]
- Guangdong Natural Science Funds [S2013050014040, 2015A030310461]
- Youth Innovation Promotion Association of CAS
Polycomb repressive complex 1 (PRC1) plays essential roles in cell-fate determination. Recent studies have found that the composition of mammalian PRC1 is particularly varied and complex; however, little is known about the functional consequences of these variant PRC1 complexes on cell-fate determination. Here, we show that Kdm2b promotes Oct4-induced somatic reprogramming through recruitment of a variant PRC1 complex (PRC1.1) to CpG islands (CGIs). Furthermore, we find that bone morphogenetic protein (BMP) represses Oct4/Kdm2b-induced somatic reprogramming selectively. Mechanistically, BMP-SMAD pathway attenuates PRC1.1 occupation and H2AK119 ubiquitination at genes linked to development, resulting in the expression of mesendodermal factors such as Sox17 and a consequent suppression of somatic reprogramming. These observations reveal that PRC1.1 participates in the establishment of pluripotency and identify BMP4 signaling as a modulator of PRC1.1 function.
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