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The Snf1 kinase and proteasome-associated Rad23 regulate UV-responsive gene expression.

ABSTRACT: The transcriptional response to damaging agents is of fundamental significance for understanding mechanisms responsible for cell survival and genome maintenance. However, how damage signals are transmitted to the transcriptional apparatus is poorly understood. Here we identify two new regulators of the UV response transcriptome: Snf1, a nutrient-sensing kinase, and Rad23, a nucleotide excision repair factor with no previously known function in transcriptional control. Over half of all UV-responsive genes are dependent on Snf1 or Rad23 for proper regulation. After irradiation, Snf1 targets the Mig3 repressor, a new effector of the UV response. Snf1 and Rad23 are both required for the displacement of Mig3 from the UV-activated HUG1 promoter, and Rad23's activity is functionally linked to the proteasome 19S regulatory particle. Our data reveal overlapping functions for Snf1 and Rad23 in UV-responsive transcriptional regulation and provide mechanistic insight into the action of these factors at a UV-activated promoter. These results also highlight how diverse environmental stimuli are processed by a limited repertoire of signalling molecules to result in tailored patterns of gene expression.

SUBMITTER: Wade SL

PROVIDER: S-EPMC2760106 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature

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The Snf1 kinase and proteasome-associated Rad23 regulate UV-responsive gene expression.

Wade Staton L SL Poorey Kunal K Bekiranov Stefan S Auble David T DT

The EMBO journal 20090813 19

The transcriptional response to damaging agents is of fundamental significance for understanding mechanisms responsible for cell survival and genome maintenance. However, how damage signals are transmitted to the transcriptional apparatus is poorly understood. Here we identify two new regulators of the UV response transcriptome: Snf1, a nutrient-sensing kinase, and Rad23, a nucleotide excision repair factor with no previously known function in transcriptional control. Over half of all UV-respons ...[more]

PMID: 19680226

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Project description:The Rad23/Rad4 protein complex plays a major role in DNA damage recognition during nucleotide excision repair (NER) in yeast. We recently showed that two distinct pathways contribute to efficient NER in yeast. The first operates independently of de novo protein synthesis and requires a nonproteolytic function of the 19S regulatory complex of the 26S proteasome and Rad23. The second pathway requires de novo protein synthesis, and relies on the activity of a newly identified Rad7-containing E3 ubiquitin ligase that ubiquitinates Rad4 in response to UV. Surprisingly, we found that cells deleted of either Rad23 or Rad4 caused reduced Rad4 and Rad23 mRNA levels respectively. We considered the possibility of an unexpected role of Rad23 and Rad4 in regulating the expression of genes involved in the transcriptional response to DNA damage. Gene expression profiling has suggested that Rad23 and Rad4 may function as a complex to affect transcription of a small subset of genes in response to UV damage. To determine how Rad4 and Rad23 contribute to the regulation of these genes, we have examined the occupancy of Rad4/Rad23 in their promoter regions by chromatin immunoprecipitation (ChIP), both in the presence and absence of UV damage. Our preliminary ChIP data suggests that the Rad4/Rad23 complex regulates a set of genes in response to UV light. We also proposed that the transcriptional regulatory activity of the Rad4-Rad23 complex required Rad4 ubiquitination. These arrays test this theory using the psocs mutant strain, which is unable to facilitate Rad4 ubiquitination after UV irradiation. *** This Series represents the gene expression component of the study. Expression analysis was performed on the pRAD7 strain, which served as the WT control, and harboured the WT RAD7 sequence on the pRS313 plasmid, the psocs strain, which harboured the same plasmid with 2 point mutations in the RAD7 sequence that prevented post-UV Rad4 ubiquitination. Expression analysis was also conducted on a pRAD7 and psocs Strain with RAD23 deleted. Analysis was performed using untreated strains, and strains 15 minutes and 60 minutes after 100Jm-2 UV irradiation. mRNA was extracted from logaritmically growing cells.

Dataset Information

The Snf1 kinase and proteasome-associated Rad23 regulate UV-responsive gene expression.

Publications

The Snf1 kinase and proteasome-associated Rad23 regulate UV-responsive gene expression.

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