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The Snf1 kinase and proteasome-associated Rad23 regulate UV-responsive gene expression
Staton L Wade1, Kunal Poorey, Stefan Bekiranov
1Department of Biochemistry and Molecular Genetics, University of Virginia Health System, Charlottesville, VA 22908-0733, USA.
The EMBO Journal
|August 15, 2009
Summary
Two new regulators, Snf1 and Rad23, control the UV response transcriptome, impacting over half of UV-responsive genes. They work together to regulate gene expression following DNA damage.
Area of Science:
- Molecular Biology
- Genetics
- Cell Biology
Background:
- Understanding cellular responses to DNA damage is crucial for genome maintenance and survival.
- The precise mechanisms transmitting damage signals to transcriptional machinery remain largely unknown.
Purpose of the Study:
- To identify novel regulators of the UV response transcriptome.
- To elucidate the roles of Snf1 and Rad23 in transcriptional control after UV irradiation.
Main Methods:
- Gene expression analysis of UV-responsive genes.
- Investigating the interaction between Snf1, Rad23, and the Mig3 repressor.
- Promoter activity assays at UV-activated promoters.
Main Results:
- Snf1 (nutrient-sensing kinase) and Rad23 (nucleotide excision repair factor) were identified as key regulators.
- Over 50% of UV-responsive genes require Snf1 or Rad23 for proper regulation.
- Snf1 targets Mig3, which is displaced from the HUG1 promoter by Snf1 and Rad23, with Rad23 linked to the proteasome.
Conclusions:
- Snf1 and Rad23 possess overlapping functions in UV-responsive transcription.
- Mechanistic insights into the regulation of UV-activated promoters by these factors were provided.
- Demonstrated how diverse stimuli are processed through conserved signaling molecules for specific gene expression patterns.
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