Phosphorylated proteins are involved in sister-chromatid arm cohesion during meiosis I

Sister-chromatid arm cohesion is lost during the metaphase I/anaphase I tra nsition to allow homologue separation, To obtain needed information on this process we have analysed in grasshopper bivalents the sequential release o f arm cohesion in relation to the behaviour of chromatid axes. Results show that sister axes are associated during early metaphase I but separate duri ng late metaphase I leading to a concomitant change of chromosome structure that implies the loss of sister-kinetochore cohesion. Afterwards, homologu es initiate their separation asynchronously depending on their size, and nu mber and position of chiasmata. In all bivalents thin chromatin strands at the telomeres appeared as the last point of contact between sister chromati ds. Additionally, we have analysed the participation of phosphoproteins rec ognised by the MPM2 monoclonal antibody against mitotic phosphoproteins in arm cohesion in bivalents and two different kinds of univalents. Results sh ow the absence of MPM-2 phosphoproteins at the interchromatid domain in mit otic chromosomes and meiotic univalents, but their presence in metaphase I bivalents. These phosphoproteins are lost at the onset of anaphase I. Taken together, these data have prompted us to propose a 'working' model for the release of arm cohesion during meiosis I. The model suggests that MPM-2 ph osphoproteins may act as cohesive proteins associating sister axes. Their m odification, once all bivalents are correctly aligned at the metaphase plat e, would trigger a change of chromosome structure and the sequential releas e of sister-kinetochore, arm, and telomere cohesions.