Polycomb complexes act redundantly to repress genomic repeats and genes

TY - JOUR

T1 - Polycomb complexes act redundantly to repress genomic repeats and genes

AU - Leeb, Martin

AU - Pasini, Diego

AU - Novatchkova, Maria

AU - Jaritz, Markus

AU - Helin, Kristian

AU - Wutz, Anton

N1 - Keywords: Animals; Cell Differentiation; Cell Line; Embryo, Mammalian; Fluorescent Antibody Technique; Gene Silencing; Mice; Multiprotein Complexes; Pluripotent Stem Cells; Repressor Proteins; Terminal Repeat Sequences

PY - 2010/2/1

Y1 - 2010/2/1

N2 - Polycomb complexes establish chromatin modifications for maintaining gene repression and are essential for embryonic development in mice. Here we use pluripotent embryonic stem (ES) cells to demonstrate an unexpected redundancy between Polycomb-repressive complex 1 (PRC1) and PRC2 during the formation of differentiated cells. ES cells lacking the function of either PRC1 or PRC2 can differentiate into cells of the three germ layers, whereas simultaneous loss of PRC1 and PRC2 abrogates differentiation. On the molecular level, the differentiation defect is caused by the derepression of a set of genes that is redundantly repressed by PRC1 and PRC2 in ES cells. Furthermore, we find that genomic repeats are Polycomb targets and show that, in the absence of Polycomb complexes, endogenous murine leukemia virus elements can mobilize. This indicates a contribution of the Polycomb group system to the defense against parasitic DNA, and a potential role of genomic repeats in Polycomb-mediated gene regulation.

AB - Polycomb complexes establish chromatin modifications for maintaining gene repression and are essential for embryonic development in mice. Here we use pluripotent embryonic stem (ES) cells to demonstrate an unexpected redundancy between Polycomb-repressive complex 1 (PRC1) and PRC2 during the formation of differentiated cells. ES cells lacking the function of either PRC1 or PRC2 can differentiate into cells of the three germ layers, whereas simultaneous loss of PRC1 and PRC2 abrogates differentiation. On the molecular level, the differentiation defect is caused by the derepression of a set of genes that is redundantly repressed by PRC1 and PRC2 in ES cells. Furthermore, we find that genomic repeats are Polycomb targets and show that, in the absence of Polycomb complexes, endogenous murine leukemia virus elements can mobilize. This indicates a contribution of the Polycomb group system to the defense against parasitic DNA, and a potential role of genomic repeats in Polycomb-mediated gene regulation.

U2 - 10.1101/gad.544410

DO - 10.1101/gad.544410

M3 - Journal article

C2 - 20123906

SN - 0890-9369

VL - 24

SP - 265

EP - 276

JO - Genes & Development

JF - Genes & Development

IS - 3

ER -