Meiotic recombination is initiated by Spo11-generated DNA double-strand breaks (DSBs) . A fraction of total DSBs is processed into crossovers (CRs) between homologous chromosomes, which promotes their accurate segregation at meiosis I (MI) . The coordination of recombination-associated events and MI progression is governed by the “pachytene checkpoint” . In budding yeast Rad17, a component of PCNA clamp-like complex, and Pch2, an AAA-ATPase, have been implicated in this checkpoint [3–7]. We show that RAD17 and PCH2 are required for two genetically separable pathways that monitor the presence of different meiotic recombination-associated lesions: First, deletion of RAD17 or SAE2, encoding a DSB-end processing factor [8, 9], suppresses delay or arrest of MI timing when DNA repair intermediates are present. Second, deletion of PCH2 suppresses delay of MI timing when aberrant synaptonemal complex (SC) is present. Importantly, ZIP1, encoding the central element of the SC  is required for activation of the PCH2-dependent checkpoint pathway. Analysis of the rad17Δ pch2Δ double mutant revealed a redundant role for these genes in regulating inter-homolog CR formation. These findings suggest a link between the surveillance of distinct recombination-associated lesions, control of CR formation kinetics and regulation of MI timing. A PCH2-ZIP1 dependent meiotic checkpoint is likely conserved among synaptic organisms from yeast to human [6, 11].