Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis

Yu Ying Phoebe Hsieh*, Vasso Makrantoni, Daniel Robertson, Adèle L. Marston, Andrew W. Murray

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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 languageEnglish
Article numbere3000635
JournalPLoS Biology
Issue number3
Publication statusPublished - 10 Mar 2020


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