Journal
SCIENCE
Volume 312, Issue 5776, Pages 1054-1059Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1122088
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Funding
- NIEHS NIH HHS [R01 ES014811, R01 ES014811-01A1] Funding Source: Medline
- NIGMS NIH HHS [R01 GM070743-01, R01 GM070743, R01 GM070743-02] Funding Source: Medline
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Failure of cells to respond to DNA damage is a primary event associated with mutagenesis and environmental toxicity. To map the transcriptional network controlling the damage response, we measured genomewide binding locations for 30 damage-related transcription factors (TFs) after exposure of yeast to methyl-methanesulfonate (MMS). The resulting 5272 TF-target interactions revealed extensive changes in the pattern of promoter binding and identified damage-specific binding motifs. As systematic functional validation, we identified interactions for which the target changed expression in wild-type cells in response to MMS but was nonresponsive in cells lacking the TF. Validated interactions were assembled into causal pathway models that provide global hypotheses of how signaling, transcription, and phenotype are integrated after damage.
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