Liu Q~Liu B, 2020

Pubmed ID 32469861
Title Yeast mismatch repair components are required for stable inheritance of gene silencing.
Authors Qian Liu, Xuefeng Zhu, Michelle Lindström, Yonghong Shi, Ju Zheng, Xinxin Hao, Claes M Gustafsson, Beidong Liu
Abstract Alterations in epigenetic silencing have been associated with ageing and tumour formation. Although substantial efforts have been made towards understanding the mechanisms of gene silencing, novel regulators in this process remain to be identified. To systematically search for components governing epigenetic silencing, we developed a genome-wide silencing screen for yeast (Saccharomyces cerevisiae) silent mating type locus HMR. Unexpectedly, the screen identified the mismatch repair (MMR) components Pms1, Mlh1, and Msh2 as being required for silencing at this locus. We further found that the identified genes were also required for proper silencing in telomeres. More intriguingly, the MMR mutants caused a redistribution of Sir2 deacetylase, from silent mating type loci and telomeres to rDNA regions. As a consequence, acetylation levels at histone positions H3K14, H3K56, and H4K16 were increased at silent mating type loci and telomeres but were decreased in rDNA regions. Moreover, knockdown of MMR components in human HEK293T cells increased subtelomeric DUX4 gene expression. Our work reveals that MMR components are required for stable inheritance of gene silencing patterns and establishes a link between the MMR machinery and the control of epigenetic silencing.
Citation PLoS Genet 2020; 16:e1008798
Data abstract Deletion collection was screened for loss of HMR silencing (silent mating type locus).


Download the list of datasets
Paper Phenotype Condition Medium Collection Tested mutants Data Details
Liu Q~Liu B, 2020 gene silencing (HMR-URA3) standard SC - Ura hap a (post-SGA) 4,268 Discrete

Curation history

Tested strains

July 22, 2020 To request.
Oct. 15, 2020 Request sent.
Oct. 17, 2020 Loaded.
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Oct. 15, 2020 Waiting for tested.
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