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dc.contributor.authorPatra, Biranchi
dc.contributor.authorKon, Yoshiko
dc.contributor.authorYadav, Gitanjali
dc.contributor.authorSevold, Anthony W
dc.contributor.authorFrumkin, Jesse P
dc.contributor.authorVallabhajosyula, Ravishankar R
dc.contributor.authorHintze, Arend
dc.contributor.authorØstman, Bjørn
dc.contributor.authorSchossau, Jory
dc.contributor.authorBhan, Ashish
dc.contributor.authorMarzolf, Bruz
dc.contributor.authorTamashiro, Jenna K
dc.contributor.authorKaur, Amardeep
dc.contributor.authorBaliga, Nitin S
dc.contributor.authorGrayhack, Elizabeth J
dc.contributor.authorAdami, Christoph
dc.contributor.authorGalas, David J
dc.contributor.authorRaval, Alpan
dc.contributor.authorPhizicky, Eric M
dc.contributor.authorRay, Animesh
dc.date.accessioned2018-11-01T14:01:59Z
dc.date.available2018-11-01T14:01:59Z
dc.date.issued2017-01-09
dc.identifier.issn0305-1048
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/284478
dc.description.abstractGenomic robustness is the extent to which an organism has evolved to withstand the effects of deleterious mutations. We explored the extent of genomic robustness in budding yeast by genome wide dosage suppressor analysis of 53 conditional lethal mutations in cell division cycle and RNA synthesis related genes, revealing 660 suppressor interactions of which 642 are novel. This collection has several distinctive features, including high co-occurrence of mutant-suppressor pairs within protein modules, highly correlated functions between the pairs and higher diversity of functions among the co-suppressors than previously observed. Dosage suppression of essential genes encoding RNA polymerase subunits and chromosome cohesion complex suggests a surprising degree of functional plasticity of macromolecular complexes, and the existence of numerous degenerate pathways for circumventing the effects of potentially lethal mutations. These results imply that organisms and cancer are likely able to exploit the genomic robustness properties, due the persistence of cryptic gene and pathway functions, to generate variation and adapt to selective pressures.
dc.description.sponsorshipNational Science Foundation (Frontiers in Integrative Biological Research) [0527023 to D.J.G, E.J.G., E.M.P., C.A., A.Rav., A.Ray.; 0523643 to A.Rav., A.Ray.; 0941078 to A.Ray.]; National Institutes of Health [1R01GM084881-01 to A.Ray.).
dc.format.mediumPrint-Electronic
dc.languageeng
dc.publisherOxford University Press (OUP)
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectSaccharomyces cerevisiae
dc.subjectRNA Polymerase II
dc.subjectSaccharomyces cerevisiae Proteins
dc.subjectGene Expression Profiling
dc.subjectComputational Biology
dc.subjectCell Division
dc.subjectGene Expression Regulation, Fungal
dc.subjectGene Dosage
dc.subjectMutation
dc.subjectGenome, Fungal
dc.subjectGenes, Lethal
dc.subjectGene Regulatory Networks
dc.subjectGenetic Fitness
dc.titleA genome wide dosage suppressor network reveals genomic robustness.
dc.typeArticle
prism.endingPage270
prism.issueIdentifier1
prism.publicationDate2017
prism.publicationNameNucleic Acids Res
prism.startingPage255
prism.volume45
dc.identifier.doi10.17863/CAM.31854
dcterms.dateAccepted2016-11-07
rioxxterms.versionofrecord10.1093/nar/gkw1148
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2017-01
dc.contributor.orcidRay, Animesh [0000-0002-0120-5820]
dc.identifier.eissn1362-4962
rioxxterms.typeJournal Article/Review
cam.issuedOnline2016-11-29


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International