Budding yeast Hed1 down-regulates the mitotic recombination machinery when meiotic recombination is impaired

  1. Hideo Tsubouchi1 and
  2. G. Shirleen Roeder1,2,3
  1. 1 Department of Molecular, Cellular, and Developmental Biology, Howard Hughes Medical Institute, Yale University, New Haven, Connecticut 06520, USA;
  2. 2 Department of Genetics, Howard Hughes Medical Institute, Yale University, New Haven, Connecticut 06520, USA

Abstract

In budding yeast, there are two RecA homologs: Rad51 and Dmc1. While Rad51 is involved in both mitotic and meiotic recombination, Dmc1 participates specifically in meiotic recombination. Here, we describe a meiosis-specific protein (Hed1) with a novel Rad51 regulatory function. Several observations indicate that Hed1 attenuates Rad51 activity when Dmc1 is absent. First, although double-strand breaks are normally poorly repaired in the dmc1 mutant, repair becomes efficient when Hed1 is absent, and this effect depends on Rad51. Second, Rad51 and Hed1 colocalize as foci on meiotic chromosomes, and chromosomal localization of Hed1 depends on Rad51. Third, production of Hed1 in vegetative cells inhibits Rad51-dependent recombination events. Fourth, the Hed1 protein shows an interaction with Rad51 in the yeast two-hybrid protein system. We propose that Hed1 provides a mechanism to ensure the coordinated action of Rad51 and Dmc1 during meiosis, by down-regulating Rad51 activity when Dmc1 is unavailable.

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