Cell fate specification and morphogenesis are two important aspects of vulval development. After the vulval precursor cells (VPCs) have acquired their fates, the VPCs divide thrice and their descendants undergo migration, elongation and fusion at the vulval midline to form seven toroidal rings stacked one over the other in an invariant fashion (Ranjana Sharma-Kishore et. al, 1999). Recently, genetic approaches have revealed that two parallel pathways regulate vulval morphogenesis . The first pathway requires the SMP-1 Semaphorin ligand, the PLX-1 Plexin receptor and the CED-10 Rac small GTPase, while the second pathway utilizes the MIG-2 Rac small GTPase and its activator UNC-73 GEF ( Dalpe et al. 2005; Ranjana S Kishore et al. 2002) . Here, we show a role for the ROCK homolog LET-502 during vulval morphogenesis. Maternally rescued
let-502(
ok1283) animals display defects in vulval toroid formation, with evidence of abnormal lumen size. The expression of the vulval fate markers was not affected in the
let-502 (
ok1283) animals, suggesting that
let-502 does not affect VPC fate specification. Genetic epistasis reveals redundancy of LET-502 with both the SMP-1/PLX-1/CED-10 and UNC-73/MIG-2 signaling pathways. During vulval morphogenesis,
let-502 is specifically expressed in the secondary vulval cells. Analysis of the
let-502 promoter reveals spatial and temporal regulation during morphogenesis by LIN-12 Notch signaling and the transcription factor LIN-1. Accordingly,
lin-12 notch loss-of-function and
lin-1 loss-of-function mutants display defects in toroid formation similar to the defects observed in
let-502 (
ok1283) mutants. Hence, Notch signaling regulates vulval morphogenesis through the activation of
let-502 transcription.