Article

Regulation of meiotic recombination via Mek1-mediated Rad54 phosphorylation.

Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY 11794-5215, USA.
Molecular cell (impact factor: 14.61). 11/2009; 36(3):393-404. DOI:10.1016/j.molcel.2009.09.029
Source: PubMed

ABSTRACT 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.

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Keywords

binding partner
 
genetic approaches
 
homologous recombination
 
inhibition
 
interhomolog recombination
 
meiosis
 
meiosis-specific kinase Mek1
 
Mek1
 
Mek1 phosphorylation
 
mitotic cells
 
mitotic recombinase Rad51
 
negative charge
 
Rad51 activity
 
Rad51 function
 
Rad51/Rad54 complex formation
 
Rad54-independent mechanism
 
recombination partner choice
 
sister chromatids
 
suppresses engagement
 
threonine 132 attenuates complex formation