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Control of expression of cell wall stress‐induced yeast genes by transcriptional attenuation
Author(s) -
Levin David E,
Kim Ki-Young
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.232.3
Subject(s) - microbiology and biotechnology , rna polymerase ii , gene , transcription (linguistics) , transcription factor , transcriptional regulation , gene expression , biology , rna , regulation of gene expression , saccharomyces cerevisiae , genetics , promoter , linguistics , philosophy
The MAPK Mpk1 of the Cell Wall Integrity signaling pathway uses a non‐catalytic mechanism to activate transcription of cell wall stress‐induced genes by acting as a co‐transcription factor. Mpk1 serves an additional function in transcription elongation that is also independent of its catalytic activity. This function is mediated by an interaction between Mpk1 and the Paf1 subunit of the Paf1C elongation complex associated with RNA Pol II. The Mpk1‐Paf1 interaction blocks recruitment of the Sen1 termination complex to the elongating RNA Pol II, thereby preventing transcriptional attenuation shortly after initiation. Attenuation under non‐inducing conditions appears to be a mechanism to minimize basal expression of stress‐induced genes. However, under inducing conditions, attenuation must be disabled to allow gene expression. Therefore, Mpk1 serves as an attenuation‐relief factor for cell wall stress‐induced genes. We found additionally that 10% of yeast protein coding genes are subject to Sen1‐mediated attenuation control that is independent of Mpk1 and cell wall stress. This subset is highly enriched for genes induced under various stress conditions, suggesting that transcriptional attenuation is a widespread phenomenon that extends to genes induced in response to a diverse array of stress conditions.