Mammalian ISWI and SWI/SNF selectively mediate binding of distinct transcription factors.

ABSTRACT: Chromatin remodelling complexes evict, slide, insert or replace nucleosomes, which represent an intrinsic barrier for access to DNA. These remodellers function in most aspects of genome utilization including transcription-factor binding, DNA replication and repair^1,2. Although they are frequently mutated in cancer³, it remains largely unclear how the four mammalian remodeller families (SWI/SNF, ISWI, CHD and INO80) orchestrate the global organization of nucleosomes. Here we generated viable embryonic stem cells that lack SNF2H, the ATPase of ISWI complexes, enabling study of SNF2H cellular function, and contrast it to BRG1, the ATPase of SWI/SNF. Loss of SNF2H decreases nucleosomal phasing and increases linker lengths, providing in vivo evidence for an ISWI function i

SUBMITTER: Barisic D 

PROVIDER: S-EPMC6522387 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature