Nancy Kleckner

TL;DR: Analysis of the effects of a 36 bp linker insertion at site I reveals the existence of communication along and between homologs prior to DSB formation, which can explain how the sites of crossovers come to lie between the homolog axes at pachytene.

TL;DR: Pch2 promotes progression of SC-associated CO and NCO recombination complexes at a regulated early–midpachytene transition that is rate-limiting for later events; in contrast, during defective meiosis, Pch2 ensures that aberrant recombination complex fail to progress so that intermediates can be harmlessly repaired during eventual return to growth.

TL;DR: Functional interactions between DSBs and the spo76-1 mutation suggest that Spo76/Pds5p opposes local destabilization of axes at developing chiasma sites and raise the possibility of a regulatory mechanism that directly monitors the presence of chiasmata at metaphase I.

TL;DR: It is proposed that Mer3, Msh4, and Mlh1 execute all of these roles during pairing by modulating the state of nascent double-strand break/partner DNA contacts within axis-associated recombination complexes.

TL;DR: Models in which chromosome axis length would determine recombination frequency are discussed and co-variation could be established at or prior to recombination initiation via programmed double-strand breaks (DSBs), or at the time of crossover control, when a subset of DSBs is designated for future maturation as crossovers.