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进化修复:多个功能模块的改变使减数分裂黏连蛋白能够支持有丝分裂。

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

机构信息

Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, United States of America.

The Wellcome Centre for Cell Biology, University of Edinburgh, Edinburgh, United Kingdom.

出版信息

PLoS Biol. 2020 Mar 10;18(3):e3000635. doi: 10.1371/journal.pbio.3000635. eCollection 2020 Mar.

DOI:10.1371/journal.pbio.3000635
PMID:32155147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7138332/
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.

摘要

蛋白质的功能在进化过程中经常发生变化,但我们不知道当蛋白质被要求参与不同的生物学功能时,细胞如何适应。我们迫使芽殖酵母,酿酒酵母,在有丝分裂细胞周期中使用减数分裂特异性 kleisin,重组 8(Rec8),而不是它的旁系同源物,Scc1。这种干扰破坏了姐妹染色单体的连接,提前了基因组复制的时间,并将生殖适应性降低了 45%。我们进行了 15 个平行种群的 1750 代进化,大大提高了它们的适应性,并分析了进化细胞的基因型和表型。只有一个种群在 Rec8 中含有突变,但许多种群在转录中介体复合物、黏着素相关基因和诱导 S 期的细胞周期调节剂中含有突变。这些突变改善了 Rec8 表达细胞中的姐妹染色单体的黏合,并延迟了基因组复制。我们的结论是,已知和新的伙伴的变化使细胞能够利用现有的蛋白质参与新的生物学功能。

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