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The MOM1 complex recruits the RdDM machinery via MORC6 to establish de novo DNA methylation.


ABSTRACT: MOM1 is an Arabidopsis factor previously shown to mediate transcriptional silencing independent of major DNA methylation changes. Here we found that MOM1 localizes with sites of RNA-directed DNA methylation (RdDM). Tethering MOM1 with artificial zinc finger to unmethylated FWA promoter led to establishment of DNA methylation and FWA silencing. This process was blocked by mutations in components of the Pol V arm of the RdDM machinery, as well as by mutation of MORC6 . We found that at some endogenous RdDM sites, MOM1 is required to maintain DNA methylation and a closed chromatin state. In addition, efficient silencing of newly introduced FWA transgenes was impaired by mutation of MOM1 or mutation of genes encoding the MOM1 interacting PIAL1/2 proteins. In addition to RdDM sites, we identified a group of MOM1 peaks at active chromatin near genes that colocalized with MORC6. These findings demonstrate a multifaceted role of MOM1 in genome regulation.

SUBMITTER: Li Z 

PROVIDER: S-EPMC9882083 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature

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The MOM1 complex recruits the RdDM machinery via MORC6 to establish <i>de novo</i> DNA methylation.

Li Zheng Z   Wang Ming M   Zhong Zhenhui Z   Gallego-Bartolomé Javier J   Feng Suhua S   Jami-Alahmadi Yasaman Y   Wang Xinyi X   Wohlschlegel James J   Bischof Sylvain S   Long Jeffrey A JA   Jacobsen Steven E SE  

bioRxiv : the preprint server for biology 20230110


MOM1 is an <i>Arabidopsis</i> factor previously shown to mediate transcriptional silencing independent of major DNA methylation changes. Here we found that MOM1 localizes with sites of RNA-directed DNA methylation (RdDM). Tethering MOM1 with artificial zinc finger to unmethylated <i>FWA</i> promoter led to establishment of DNA methylation and <i>FWA</i> silencing. This process was blocked by mutations in components of the Pol V arm of the RdDM machinery, as well as by mutation of <i>MORC6</i> .  ...[more]

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