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Kdm2b Regulates Somatic Reprogramming through Variant PRC1 Complex-Dependent Function
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DOI：10.1016/j.celrep.2017.10.091.png)
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Abstract
En 中文
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.
Keywords:
H2A UBIQUITYLATION
CPG ISLANDS
HISTONE H3
POLYCOMB
FAMILY
PROTEINS
RYBP
DEMETHYLATION
RECRUITMENT
GENES
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