Tid1/Rdh54 promotes colocalization of Rad51 and Dmc1 during meiotic recombination

Two RecA homologs, Rad51 and Dmc1, assemble as cytologically visible comple xes (foci) at the same sites on meiotic chromosomes. Time course analysis c onfirms that co-foci appear and disappear as the single predominant form. A large fraction of co-foci are eliminated in a red1 mutant, which is expect ed as a characteristic of the interhomolog-specific recombination pathway. Previous studies suggested that normal Dmc1 loading depends on Rad51. We sh ow here that a mutation in TID1/RDH54, encoding a RAD54 homolog, reduces Ra d51-Dmc1 colocalization relative to WT. A rad54, mutation, in contrast, has relatively little effect on RecA homolog foci except when strains also con tain a tid1/rdh54 mutation the role of Tid1/Rdh54 in coordinating RecA homo log assembly may be very direct, because Tid1/Rdh54 is known to physically bind both Dmc1 and Rad51. Also, Dmc1 foci appear early in a tid1/rdh54 muta nt. Thus, Tid1 may normally act with Rad51 to promote ordered RecA homolog assembly by blocking Dmc1 until Rad51 is present. Finally, whereas double-s taining foci predominate in WT nuclei, a subset of nuclei with expanded chr omatin exhibit individual Rad51 and Dmc1 foci side-by-side, suggesting that a Rad51 homo-oligomer and a Dmc1 homo-oligomer assemble next tb one anothe r at the site of a single double-strand break (DSB) recombination intermedi ate.