Asymmetric disassembly of the synaptonemal complex (SC) is crucial for proper
meiotic chromosome segregation. However, the signaling mechanisms that directly regulate this
process are poorly understood. Here we show that the mammalian Rho GEF homolog, ECT-2,
functions through the conserved RAS/ERK MAP kinase signaling pathway in the C. elegans
germline to regulate the disassembly of SC proteins. We find that SYP-2, a SC central region
component, is a potential target for MPK-1-mediated phosphorylation and that constitutively
phosphorylated SYP-2 impairs the disassembly of SC proteins from chromosomal domains referred
to as the long arms of the bivalents. Inactivation of MAP kinase at late pachytene is critical for
timely disassembly of the SC proteins from the long arms, and is dependent on the crossover (CO)
promoting factors ZHP-3/RNF212/Zip3 and COSA-1/CNTD1. We propose that the conserved MAP
kinase pathway coordinates CO designation with the disassembly of SC proteins to ensure accurate
chromosome segregation.