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Rewiring of genetic networks in response to DNA damage.

Authors
Type
Published Article
Journal
Science
0036-8075
Publisher
American Association for the Advancement of Science (AAAS)
Volume
330
Issue
6009
Pages
1385–1389
Identifiers
DOI: 10.1126/science.1195618
Source
Ideker Lab

Abstract

Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping, we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases, and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3 phosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized. Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli.

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