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MOM1 and Pol‐IV/V interactions regulate the intensity and specificity of transcriptional gene silencing
Author(s) -
Yokthongwattana Chotika,
Bucher Etienne,
Čaikovski Marian,
Vaillant Isabelle,
Nicolet Joël,
Scheid Ortrun Mittelsten,
Paszkowski Jerzy
Publication year - 2010
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2009.328
Subject(s) - biology , heterochromatin , gene silencing , genetics , rna polymerase iii , epigenetics , transcription (linguistics) , rna polymerase ii , enhancer , transcriptional regulation , rna induced transcriptional silencing , regulation of gene expression , gene , microbiology and biotechnology , transcription factor , rna polymerase , rna interference , chromatin , gene expression , rna , promoter , linguistics , philosophy
It is commonly observed that onset or release of transcriptional gene silencing (TGS) correlates with alteration of repressive epigenetic marks. The TGS regulator MOM1 in Arabidopsis is exceptional since it regulates transcription in intermediate heterochromatin with only minor changes in epigenetic marks. We have isolated an enhancer of the mom1 mutation that points towards regulatory interplay between MOM1 and RNA polymerase‐V (Pol‐V). Pol‐V transcribes heterochromatic loci, which seems to be required for maintenance of their silencing; however, 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 genetically interacts with MOM1 in the control of gene silencing. Interestingly, functional cooperation of MOM1 and Pol‐V not only broadens the range of the controlled loci in comparison to each individual factor, but also determines the degree of TGS.