Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The SUMO E3 ligase-like proteins PIAL1 and PIAL2 interact with MOM1 and form a novel complex required for transcriptional silencing [RNA-seq]

ABSTRACT: The mechanism by which MORPHEUS'MOLECULE1 (MOM1) contributes to transcriptional gene silencing remained elusive since the gene was first identified and characterized (Amedeo et al., 2000). Here, we report that two PIAS (PROTEIN INHIBITOR OF ACTIVATED STAT)-type SUMO E3 ligase-like proteins PIAL1 and PIAL2 function redundantly to mediate transcriptional silencing at MOM1 target loci. PIAL1 and PIAL2 physically interact with each other and with MOM1 to form a high-molecular-weight complex. In the absence of either PIAL2 or MOM1, the formation of the high-molecular-weight complex was disrupted. We identified a previously uncharacterized IND (interacting domain) in PIAL1 and PIAL2, and demonstrated that IND directly interacts with MOM1. The CMM2 (conserved MOM1 motif 2) domain of MOM1 was previously shown to be required for the dimerization of MOM1. We demonstrated that the CMM2 domain is also required for the interaction of MOM1 with PIAL1 and PIAL2. We found that although PIAL2 has a SUMO E3 ligase activity, the activity is dispensable for PIAL2 in transcriptional silencing. This study suggests that PIAL1 and PIAl2 act as components of the MOM1-containing complex to mediate transcriptional silencing at heterochromatin regions.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE80301 | GEO | 2016/04/15

SECONDARY ACCESSION(S): PRJNA318519

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The SUMO E3 ligase-like proteins PIAL1 and PIAL2 interact with MOM1 and form a novel complex required for transcriptional silencing [Bisulfite-seq]

Project description:The mechanism by which MORPHEUS'MOLECULE1 (MOM1) contributes to transcriptional gene silencing remained elusive since the gene was first identified and characterized (Amedeo et al., 2000). Here, we report that two PIAS (PROTEIN INHIBITOR OF ACTIVATED STAT)-type SUMO E3 ligase-like proteins PIAL1 and PIAL2 function redundantly to mediate transcriptional silencing at MOM1 target loci. PIAL1 and PIAL2 physically interact with each other and with MOM1 to form a high-molecular-weight complex. In the absence of either PIAL2 or MOM1, the formation of the high-molecular-weight complex was disrupted. We identified a previously uncharacterized IND (interacting domain) in PIAL1 and PIAL2, and demonstrated that IND directly interacts with MOM1. The CMM2 (conserved MOM1 motif 2) domain of MOM1 was previously shown to be required for the dimerization of MOM1. We demonstrated that the CMM2 domain is also required for the interaction of MOM1 with PIAL1 and PIAL2. We found that although PIAL2 has a SUMO E3 ligase activity, the activity is dispensable for PIAL2 in transcriptional silencing. This study suggests that PIAL1 and PIAl2 act as components of the MOM1-containing complex to mediate transcriptional silencing at heterochromatin regions.

2016-04-15 | GSE80302 | GEO

The SUMO E3 ligase-like proteins PIAL1 and PIAL2 interact with MOM1 and form a novel complex required for transcriptional silencing

Project description:The SUMO E3 ligase-like proteins PIAL1 and PIAL2 interact with MOM1 and form a novel complex required for transcriptional silencing

| PRJNA318515 | ENA

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

Project description: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.

2023-06-10 | PXD039991 | Pride

Sumoylation at Chromatin Governs Coordinated Repression of a Transcriptionnal Program Essential for Cell Growth and Proliferation

Project description:mRNA profiling of WI38 wild-type or overexpressiong the SUMO E3 ligase PIASy in human primary fibroblasts 24h post-infection. The goal of this study is to analyse transcriptional changes in cells over-expressing the SUMO E3 ligase PIASy and to compare them with ChIPseq data for several histones marks and proteins of the SUMO machinery including PIASy

2013-11-25 | E-MEXP-3776 | biostudies-arrayexpress

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

Project description: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, again colocalized with MORC6. These findings demonstrate a multifaceted role of MOM1 in genome regulation.

2023-06-09 | GSE221679 | GEO

Transcriptional gene silencing mediated by interplay of MOM1 and Pol V

Project description:In plants, multiple levels of epigenetic control suppress transposon movement and permit somatic as well as transgenerational transmission of gene expression patterns. A variety of factors are involved that establish and/or maintain epigenetic marks, such as covalent modification of DNA and histones. Alteration of epigenetic marks leads to the enhancement or release of transcriptional gene silencing (TGS). TGS regulator MOM1 is special in this respect since it silences transcription by an unknown mechanism operating without obvious changes in epigenetic marks. We have isolated an enhancer of the mom1 mutation that points towards regulatory interplay between MOM1 and the plant-specific RNA Polymerase V (Pol V). Pol V transcribes heterochromatic loci and silences them. Although its biochemical properties have been studied; it is still not clear how Pol V is targeted to heterochromatin. We now provide evidence that Pol V is required for MOM1-mediated suppression of transcription at a subset of its chromosomal targets. Thus, Pol V interacts with MOM1 in the control of gene silencing. Interestingly, functional relationships between mutations in MOM1 and Pol V genes range from enhancement to independence or even suppression at different target loci.

2009-11-24 | GSE17940 | GEO

Transcriptional gene silencing mediated by interplay of MOM1 and Pol V

2010-06-19 | E-GEOD-17940 | biostudies-arrayexpress

Expression data for the mom1-2 mutant of Arabidopsis

Project description:Heterochromatin is an inert region in the genome and composed of mainly remnants of transposons and repetitive elements. In Arabidopsis, the major heterchromatin regions are present at around centromeres (pericentromeric regions) and at a region on the short arm of chromosome 4 (heterochromatin knob). Histones and DNAs in heterochromatin have characteristic features with abundant H3H9me2 and cytosine methylation, respectively. Here, by using a genome tiling array, we showed that a subset of heterochromatin loci are silenced by the action of Morpheus' molecule 1 (MOM1) that is an epigeneic regulator for transcriptional gene silencing independent of global DNA and histone modification. Most of the up-regulated loci in the mom1 mutant carried sequences related to transposable elements but none of them was annotated as functional transposons. No specific subclass of transposons was targeted by MOM1 and loci that were unrelated to transposons but flanked by short tandem repeats were also shown to be under the control of MOM1. The results suggest the presence of an unknown level of regulatory network maintaining the silent state of heterochromain in the genome. Keywords: Epigenetic regulation of endogenous loci by Morpheus' Molecule 1 (MOM1)

2010-09-27 | GSE13092 | GEO

Expression data for the mom1-2 mutant of Arabidopsis

2010-09-26 | E-GEOD-13092 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:The SUMO E3 ligase-like proteins PIAL1 and PIAL2 interact with MOM1 and form a novel complex required for transcriptional silencing [Bisulfite-seq]

| PRJNA318520 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data