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The pluripotency factor Nanog regulates pericentromeric heterochromatin
organization in mouse embryonic stem cells
#MMPMID27125671
Novo CL
; Tang C
; Ahmed K
; Djuric U
; Fussner E
; Mullin NP
; Morgan NP
; Hayre J
; Sienerth AR
; Elderkin S
; Nishinakamura R
; Chambers I
; Ellis J
; Bazett-Jones DP
; Rugg-Gunn PJ
Genes Dev
2016[May]; 30
(9
): 1101-15
PMID27125671
show ga
An open and decondensed chromatin organization is a defining property of
pluripotency. Several epigenetic regulators have been implicated in maintaining
an open chromatin organization, but how these processes are connected to the
pluripotency network is unknown. Here, we identified a new role for the
transcription factor NANOG as a key regulator connecting the pluripotency network
with constitutive heterochromatin organization in mouse embryonic stem cells.
Deletion of Nanog leads to chromatin compaction and the remodeling of
heterochromatin domains. Forced expression of NANOG in epiblast stem cells is
sufficient to decompact chromatin. NANOG associates with satellite repeats within
heterochromatin domains, contributing to an architecture characterized by highly
dispersed chromatin fibers, low levels of H3K9me3, and high major satellite
transcription, and the strong transactivation domain of NANOG is required for
this organization. The heterochromatin-associated protein SALL1 is a direct
cofactor for NANOG, and loss of Sall1 recapitulates the Nanog-null phenotype, but
the loss of Sall1 can be circumvented through direct recruitment of the NANOG
transactivation domain to major satellites. These results establish a direct
connection between the pluripotency network and chromatin organization and
emphasize that maintaining an open heterochromatin architecture is a highly
regulated process in embryonic stem cells.
|Animals
[MESH]
|Cell Line
[MESH]
|Chromatin Assembly and Disassembly/genetics
[MESH]
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