Roles for two RecA homologs in promoting meiotic chromosome synapsis.

Abstract

Previous studies have shown that the RAD51 and DMCl genes of Saccharomyces cerevisiae encode homologs of the Escherichia coli RecA strand exchange enzyme. Results presented here demonstrate that the dmcl and radSl mutants undergo nearly complete chromosome synapsis, but synaptonemal complex formation is delayed substantially compared with wild type. In the zipl mutant, chromosomes are paired homologously, but not synapsed, and the protein backbones (axial elements] of each pair of chromosomes are connected intimately to each other at a few sites referred to herein as axial associations, dmcl zipl and radSl zipl double mutants assemble axial elements that are not obviously associated, demonstrating that the Dmcl and Rad51 proteins are required to establish or stabilize axial associations. We propose that axial associations serve to promote meiotic chromosome synapsis and that the absence of these associations accounts for the delayed and inefficient synapsis observed in dmcl and radSl strains. During meiosis in haploid yeast, chromosome synapsis takes place between nonhomologous chromosome segments. In a zipl haploid, axial associations are not apparent, suggesting that these associations depend on interactions between homologous sequences.

Red-Hed regulation: recombinase Rad51, though capable of playing the leading role, may be relegated to supporting Dmc1 in budding yeast meiosis: Figure 1.

“…These results are consistent with a single pathway in which the functions of the two recombinases are interdependent. Both recombinases are needed for the interhomolog connections between paired axial elements that are seen in SCdefective zip1 mutants, again consistent with cooperation of the recombinases (Rockmill et al 1995). Finally, analysis of Rad51-and Dmc1-dependent recombination intermediates provided evidence that unique functions of Rad51 and Dmc1 contribute to normal progression of a recombination event (Schwacha and Kleckner 1997).…”

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

“…Physical analysis has shown that DSBs are very rapidly repaired after the reintroduction of nutrients that support mitotic growth (Schwacha & Kleckner 1997;Zenvirth et al 1997). Restoration of viability and repair of DSBs in dmc1 following return to growth requires both RAD51 (Rockmill et al 1995;Dresser et al 1997;Schwacha & Kleckner 1997;Zenvirth et al 1997), and RAD54 (this work). A second situation in which normal levels of RAD54 are suf®cient for complete or nearly complete DMC1-independent resolution of DSBs is in a red1 mutant background.…”

“…Again, DMC1-independent recombination depends largely on the function of DMC1's relative, RAD51 (Rockmill et al 1995;Dresser et al 1997;Schwacha & Kleckner 1997;. Clari®cation of the relationship of Rad54 and Dmc1 function was afforded by discovery of the TID1/RDH54 gene (Dresser et al 1997;Klein 1997;M.…”

Saccharomyces cerevisiae recA homologues RAD51 and DMC1 have both distinct and overlapping roles in meiotic recombination

“…On the other hand, Rockmill et al (1995) have proposed that Dmc1 is involved in structural events that indirectly promote recombination. This work suggests that Dmc1 and Rad51 share a recombinogenic function.…”