Sustained and rapid chromosome movements are critical for chromosome pairing and meiotic progression in budding XXXX .

@entity375 @entity73278 @entity374 @entity493 @entity20088
Telomere-led chromosome movements are a conserved feature of meiosis I (MI) prophase. Several roles have been proposed for such chromosome motion, including promoting homolog pairing and removing inappropriate chromosomal interactions. Here, we provide evidence in budding @entity375 that rapid chromosome movements affect homolog pairing and recombination. We found that @entity73278 /\ strains, which are defective for telomere-led chromosome movements, show defects in homolog pairing as measured in a "one-dot/two-dot tetR-GFP" assay; however, pairing in @entity73278 /\ eventually reaches near wild-type (WT) levels. Charged-to- @entity493 scanning mutagenesis of @entity73278 yielded one allele, @entity73278 -3, that confers a @entity73278 /\-like delay in meiotic prophase but promotes high spore viability. The meiotic delay in @entity73278 -3 strains is essential for spore viability because a null mutation ( @entity20088 /\) in the @entity20088 checkpoint protein suppresses the delay but confers a severe spore viability defect. @entity73278 -3 mutants show a general defect in chromosome motion but an intermediate defect in chromosome pairing. Chromosome velocity analysis in live cells showed that while average chromosome velocity was strongly reduced in @entity73278 -3, chromosomes in this mutant displayed occasional rapid movements. Lastly, we observed that @entity374 mutants displaying lower levels of meiosis-induced double-strand breaks showed higher spore viability in the presence of the @entity73278 -3 mutation compared to @entity73278 /\. On the basis of these observations, we propose that during meiotic prophase the presence of occasional fast moving chromosomes over an extended period of time is sufficient to promote WT levels of recombination and high spore viability; however, sustained and rapid chromosome movements are required to prevent a checkpoint response and promote efficient meiotic progression.
