Transcriptional gene silencing by Arabidopsis microrchidia homologues involves the formation of heteromers

Guillaume Moissiard, Sylvain Bischof, Dylan Husmann, William A. Pastor, Christopher J. Hale, Linda Yen, Hume Stroud, Ashot Papikian, Ajay A. Vashisht, James A. Wohlschlegel, Steven E. Jacobsen

Research output: Contribution to journalArticlepeer-review

Abstract

Epigenetic gene silencing is of central importance to maintain genome integrity and is mediated by an elaborate interplay between DNA methylation, histone posttranslational modifications, and chromatin remodeling complexes. DNA methylation and repressive histone marks usually correlate with transcriptionally silent heterochromatin, however there are exceptions to this relationship. In Arabidopsis, mutation of Morpheus Molecule 1 (MOM1) causes transcriptional derepression of heterochromatin independently of changes in DNA methylation. More recently, two Arabidopsis homologues of mouse microrchidia (MORC) genes have also been implicated in gene silencing and heterochromatin condensation without altering genome-wide DNA methylation patterns. In this study, we show that Arabidopsis microrchidia (AtMORC6) physically interacts with AtMORC1 and with its close homologue, AtMORC2, in two mutually exclusive protein complexes. RNA-sequencing analyses of high-order mutants indicate that AtMORC1 and AtMORC2 act redundantly to repress a common set of loci. We also examined genetic interactions between AtMORC6 and MOM1 pathways. Although AtMORC6 and MOM1 control the silencing of a very similar set of genomic loci, we observed synergistic transcriptional regulation in the mom1/atmorc6 double mutant, suggesting that these epigenetic regulators act mainly by different silencing mechanisms.

Original languageEnglish (US)
Pages (from-to)7474-7479
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume111
Issue number20
DOIs
StatePublished - May 20 2014
Externally publishedYes

ASJC Scopus subject areas

  • General

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