Spo11-induced meiotic DNA double-strand breaks (DNA DSBs) couple uncoupling of nonhomologous centromere (CEN) pairs with SC formation between homologous chromosomes, in budding yeast meiosis. CEN coupling and uncoupling depend upon the phosphorylation state of Zip1, respectively, regulated by the PP4 phosphatase and Mec1 kinase activities. Nonhomologous CENs are coupled in early meiosis (leptotene), prior to Spo11-induced generation of DSBs. DSB-dependent activation of Mec1 and resultant Zip1-phosphorylation (Zip1-P) lead to uncoupling of the nonhomologous CENs [8]. By this stage, coupling and uncoupling are likely in dynamic equilibrium [5, 8]. DSBs are repaired by crossover (CO) or noncrossover (NCO) recombination pathways. Interhomolog CO recombination leads to the localization of Synapsis Initiation Complex (SIC) at the sites of CO and consequent SC-initiation from the CO sites, in zygotene [21, 22]. CO recombination and SC formation between the homologous chromosomes may sequester the homologous CENs from cycles of coupling-uncoupling and facilitate Zip1-dependent coupling of the homologous CENs [23, 24], owing to PP4 activity and inhibition of further Mec1 activation. In addition to the CO sites, coupled CENs, both homologous and nonhomologous, are potent sites of SC initiation [23, 25]. SC initiation from the nonhomologously coupled CENs is prevented by the combined actions of Zip3 and Fpr3 which probably act in separate pathways [25]. Inhibition of the centromeric SC initiation by Zip3 and Fpr3 is relieved upon DNA DSB formation, the mechanism of which is unclear, allowing SC initiation from the homologously coupled CENs. Steps in red are postulated. Steps inside the blue box are largely absent in spo11 mutant. Note that the relationship between SC initiations at the centromere and at CO site is unclear, and alternate models are proposed in Figure 4.