Causal role for inheritance of H3K27me3 in maintaining the OFF state of a Drosophila HOX gene

Author:

Coleman Rory T.1ORCID,Struhl Gary1ORCID

Affiliation:

1. Department of Genetics and Development, Columbia University College of Physicians and Surgeons, 701 West 168th Street, New York, NY 10032, USA.

Abstract

DNA sequence and inherited gene silencing Cell fate decisions require a gene's transcriptional status, whether on or off, to be stably and heritably maintained over multiple cell generations. For silenced genes, heterochromatin domains are associated with specific histone posttranslational modifications, and these histone marks are maintained during DNA replication and chromosome duplication (see the Perspective by De and Kassis). Laprell et al. show that parental methylated histone H3 lysine 27 (H3K27) nucleosomes in Drosophila are inherited in daughter cells after replication and can repress transcription, but that they are not sufficient to propagate the mark. Trimethylation of newly incorporated nucleosomes requires recruitment of the methyltransferase Polycomb repressive complex 2 (PRC2) to neighboring cis-regulatory DNA elements. Coleman and Struhl demonstrate that H3K27 trimethylated nucleosomes play a causal role in transmitting epigenetic memory at a Drosophila HOX gene through anchoring of PRC2 at the Polycomb response element binding site. Wang and Moazed examine fission yeast and show that both sequence-dependent and chromodomain sequence-independent mechanisms are required for stable epigenetic inheritance of histone modifications and the epigenetic maintenance of silencing. These studies highlight the crucial role of DNA binding for heritable gene silencing during growth and development. Science , this issue p. 85 , p. eaai8236 , p. 88 ; see also p. 28

Funder

National Institutes of Health

Howard Hughes Medical Institute

Ellison Medical Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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