Regulation of Meiotic Recombination via Mek1-Mediated Rad54 Phosphorylation

Hengyao Niu, Lihong Wan, Valeria Busygina, Young Ho Kwon, Jasmina A. Allen, Xue Li, Ryan C. Kunz, Kazuishi Kubota, Beatrice Wang, Patrick Sung, Kevan M. Shokat, Steven P. Gygi, Nancy M. Hollingsworth

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130 Scopus citations


A preference for homologs over sister chromatids in homologous recombination is a fundamental difference in meiotic versus mitotic cells. In budding yeast, the bias for interhomolog recombination in meiosis requires the Dmc1 recombinase and the meiosis-specific kinase Mek1, which suppresses engagement of sister chromatids by the mitotic recombinase Rad51. Here, a combination of proteomic, biochemical, and genetic approaches has identified an additional role for Mek1 in inhibiting the activity of the Rad51 recombinase through phosphorylation of its binding partner, Rad54. Rad54 phosphorylation of threonine 132 attenuates complex formation with Rad51, and a negative charge at this position reduces Rad51 function in vitro and in vivo. Thus, Mek1 phosphorylation provides a dynamic means of controlling recombination partner choice in meiosis in two ways: (1) it reduces Rad51 activity through inhibition of Rad51/Rad54 complex formation, and (2) it suppresses Rad51-mediated strand invasion of sister chromatids via a Rad54-independent mechanism.

Original languageEnglish (US)
Pages (from-to)393-404
Number of pages12
JournalMolecular Cell
Issue number3
StatePublished - Nov 13 2009
Externally publishedYes


  • DNA

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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