Projects per year
Abstract
The role of proteins often changes during evolution, but we do not know how cells adapt when a protein is asked to participate in a different biological function. We forced the budding yeast, Saccharomyces cerevisiae, to use the meiosis-specific kleisin, recombination 8 (Rec8), during the mitotic cell cycle, instead of its paralog, Scc1. This perturbation impairs sister chromosome linkage, advances the timing of genome replication, and reduces reproductive fitness by 45%. We evolved 15 parallel populations for 1,750 generations, substantially increasing their fitness, and analyzed the genotypes and phenotypes of the evolved cells. Only one population contained a mutation in Rec8, but many populations had mutations in the transcriptional mediator complex, cohesin-related genes, and cell cycle regulators that induce S phase. These mutations improve sister chromosome cohesion and delay genome replication in Rec8-expressing cells. We conclude that changes in known and novel partners allow cells to use an existing protein to participate in new biological functions.
Original language | English |
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Article number | e3000635 |
Journal | PLoS Biology |
Volume | 18 |
Issue number | 3 |
DOIs | |
Publication status | Published - 10 Mar 2020 |
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Dive into the research topics of 'Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis'. Together they form a unique fingerprint.Projects
- 3 Finished
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`Core Funding for the Wellcome Trust Centre for Cell Biology¿, Research Enrichment, Public Engagement
Tollervey, D. (Principal Investigator)
1/12/18 → 1/06/22
Project: Research
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Wellcome Centre for Cell Biology
Tollervey, D. (Principal Investigator)
1/12/16 → 1/12/21
Project: Research
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Mechanisms orienting chromosomes in mitosis and meiosis
Marston, A. (Principal Investigator)
1/03/16 → 28/08/21
Project: Research