| Literature DB >> 27811238 |
Jolanda van Leeuwen1, Carles Pons2,3, Joseph C Mellor1,4, Takafumi N Yamaguchi1,4,5, Helena Friesen1, John Koschwanez6, Mojca Mattiazzi Ušaj1, Maria Pechlaner7, Mehmet Takar8, Matej Ušaj1, Benjamin VanderSluis2, Kerry Andrusiak1,5, Pritpal Bansal1,4, Anastasia Baryshnikova9, Claire E Boone1, Jessica Cao1, Atina Cote1,4, Marinella Gebbia1,4, Gene Horecka1, Ira Horecka1, Elena Kuzmin1,5, Nicole Legro1, Wendy Liang1, Natascha van Lieshout1,4,5, Margaret McNee1, Bryan-Joseph San Luis1, Fatemeh Shaeri1,4, Ermira Shuteriqi1, Song Sun1, Lu Yang1, Ji-Young Youn4, Michael Yuen1, Michael Costanzo1, Anne-Claude Gingras4,5, Patrick Aloy3,10, Chris Oostenbrink7, Andrew Murray6, Todd R Graham8, Chad L Myers11,12, Brenda J Andrews13,5, Frederick P Roth13,4,5,12,14, Charles Boone13,5,12.
Abstract
Genetic suppression occurs when the phenotypic defects caused by a mutation in a particular gene are rescued by a mutation in a second gene. To explore the principles of genetic suppression, we examined both literature-curated and unbiased experimental data, involving systematic genetic mapping and whole-genome sequencing, to generate a large-scale suppression network among yeast genes. Most suppression pairs identified novel relationships among functionally related genes, providing new insights into the functional wiring diagram of the cell. In addition to suppressor mutations, we identified frequent secondary mutations,in a subset of genes, that likely cause a delay in the onset of stationary phase, which appears to promote their enrichment within a propagating population. These findings allow us to formulate and quantify general mechanisms of genetic suppression.Entities:
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Year: 2016 PMID： 27811238 PMCID： PMC5562937 DOI： 10.1126/science.aag0839
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728