Like several other organisms, budding yeast has been shown to exhibit a period in which centromeres become grouped in a homology independent fashion 
. Zip1 was shown to play a role in this phenomenon 
. These first studies used a single time point analysis to evaluate centromere-coupling. The analysis revealed key features of the centromere coupling phenomenon in budding yeast, but left unanswered questions related to the timing of the phenomenon, an issue that has been difficult to address in other systems in which homology-independent meiotic centromere interactions have been reported. We have used this approach to directly position centromere coupling in relation to other meiotic events, study its dynamics and better understand the role of Zip1 in this phenomenon.
As demonstrated previously 
, we found that centromere coupling unequivocally takes place before SC formation. The tight centromere clusters that typify cells entering the meiotic program are largely maintained through S-phase and centromeres then transition quickly into non-homologous pairs. It is not clear whether centromeres emerge from the clusters as couples, disperse from the clusters and then become coupled, or both. Individual centromeres clearly do not linger long between clustering and coupling. Cells with these dispersed centromeres were observed, but at very low frequencies. Similarly we do not observe a stage of dispersed centromeres between coupling and homologous pairing. Thus the transition from non-homologous to homologous partners may be brief, or centromere coupling may be dynamic process, as suggested by Tsubouchi and Roeder 
such that not all the centromeres disengage from their partners simultaneously.
We have studied the dynamics of centromere coupling in spo11Δ mutants. We have observed that the process is dramatically affected by the SPO11 deletion; centromere coupling persists at all times evaluated. Thus, SPO11 is required, at least indirectly, for the transition from non-homologous coupling to homologous pairing of the centromeres, suggesting a connection between events promoted by Spo11 activity, presumably through the formation of double strand breaks, and a triggered release from coupling after homologous recombination is initiated.
Zip1 is the structural element that holds the lateral elements of the SC together 
. Zip1 could be imagined to perform a similar role during centromere coupling by bridging the centromeres of non-homologous chromosomes. Our results showing that centromere coupling is abolished at all time points in zip1
deletion mutants are consistent with this sort of direct structural role for Zip1. However, the formal possibility remains that centromeres still couple in zip1Δ
cells, but the engagements are short-lived and not detectable with our experimental approach. If Zip1 is the structural element holding centromeres together, Zip1 should localize to the centromeres when they are coupled. We have observed more variable numbers and intensities of punctate Zip1 foci and a lower incidence of Zip1/kinetchore co-localization than previous studies. It seems from these observations and work of others 
that 1) Zip1 may localize to more than just centromere regions in early meiosis, and 2) that relatively small (undetectable in our assays) amounts of Zip1 may be sufficient to promote coupling.
What is the role of centromere coupling? Centromere coupling has been proposed to promote homologous pairing by holding the centromeres of two chromosomes together while homology at the arms is being assessed 
. However, ZIP1
deletion mutants do not have dramatic pairing defects along the chromosome arms 
and some studies suggest that the bringing together of homologous centromeres is dependent upon interactions between the arms 
. The results here suggest an alternative possibility; centromere coupling might be preventing the formation of deleterious crossing-over at the centromere. A recent analysis of the global distribution of meiotic crossovers in budding yeast suggested that Zip1 is necessary for the repression of centromeric crossing-over 
. The authors concluded that Zip1, in some way, directs DSBs repair towards the sister chromatids. We have shown that centromere coupling initiates prior to the association of Dmc1 with the chromosomes and that Dmc1 loading occurs when centromeres are coupled with non-homologous partners. This suggests that Zip1 may be manifesting its role in centromere crossover repression by coupling centromeres with non homologous partners. We propose two different mechanisms by which the coupling process might play this role. First, the sequestration of centromeres with non-homologous partners (, centromere sequestration) may spatially or topologically prevent interactions between homologous centromere regions, leaving sister chromatids as default partners for repairing DSBs (, recombination complex marked with an asterisk). Alternatively, (, crossover inhibition) Zip1 could promote inter-sister over inter-homolog repair of DSBs by blocking the recruitment, or affecting the function, of components of the recombination process that are required for interhomolog events (, crossover inhibition, orange circles). It has been noted that in early prophase Dmc1 and Zip1 foci are non-overlapping, consistent with the notion that Zip1 deposition may exclude components of the recombination machinery 
. By this model, centromere coupling might act to increase the polymerization or stability of Zip1 around the centromeres or could be an innocuous by-product of Zip1 assembly properties.