Begley TJ~Samson LD, 2004

Pubmed ID 15469827
Title Hot spots for modulating toxicity identified by genomic phenotyping and localization mapping.
Authors Thomas J Begley, Ari S Rosenbach, Trey Ideker, Leona D Samson
Abstract DNA repair and checkpoint pathways protect against carcinogen-induced toxicity. Here, we describe additional, equally protective pathways discovered by interrogating 4,733 yeast proteins for their ability to diminish toxicity induced by four known carcinogens. A computational mapping strategy for global phenotypic data was developed to build a systems toxicology model detailing recovery from carcinogen exposure and identifying protein complexes that modulate toxicity. Global phenotypic data were merged with global subcellular localization and protein interactome data to generate an integrated picture of cellular recovery after carcinogen exposure. Statistically validated results from this systems-wide integration demonstrate that, in addition to the nucleus, subnetworks of toxicity-modulating proteins were overrepresented in the vacuolar membrane, endosome, endoplasmic reticulum, and mitochondrion. In addition, we show that many proteins associated with RNA polymerase II, macromolecular trafficking, and vacuole function can now be counted among the many proteins that modulate carcinogen-induced toxicity.
Citation Mol. Cell 2004; 16:117-25


Download the list of datasets
Papers Phenotype Conditions Collection Tested mutants Data Details
Begley TJ~Samson LD, 2004 growth (spot assay) methylmethane sulphonate [0.01-0.03%] hap a 4,784 Discrete
Begley TJ~Samson LD, 2004 growth (spot assay) t-BuOOH [0.50-1.25 mM] hap a 4,784 Discrete
Begley TJ~Samson LD, 2004 growth (spot assay) 4-nitroquinoline N-oxide [0.2-0.5 ug/ml] hap a 4,784 Discrete
Begley TJ~Samson LD, 2004 growth (spot assay) ultraviolet light [40-125 J/m2] hap a 4,784 Discrete

Curation history

April 5, 2013 Data requested.
April 19, 2013 Data requested.
May 28, 2014 Tested strains loaded.
May 28, 2014 Data abandoned.
May 28, 2014 Data loaded.