Many developmental systems appear insensitive to a certain degree of perturbation. For instance, the output of vulval cell fate patterning is quasi-invariant among several C. elegans wild isolates grown in different conditions. In theory, a system robust to environmental perturbations could also be robust to certain genetic mutations. Consequently, even if the final product is constant, the signaling network involved in its development may accumulate cryptic genetic variation within species. Previously, the presence of cryptic genetic variation affecting the activity of the vulval signaling network within C. elegans species was uncovered through several approaches (Milloz et al., Genes & Dev. , 2008). One of them was to introduce a mutation affecting vulval cell fate induction into different C. elegans wild isolates. For instance, the
let-23(
sy1) allele of EGFR causes stronger defect of vulva induction in N2 than in AB1 genetic background, revealing the presence of cryptic genetic variation. In the work presented here, we attempt to characterize the genetic architecture of this cryptic variation and to identify the underlying molecular variation . A Quantitative Trait Locus analysis performed from the genotypes and phenotypes of 60 Recombinant Inbred Lines detected one major-effect locus on chromosome I. By constructing several Near-Isogenic Lines, we further mapped this locus to a 273 kb genomic interval. Only three N2/AB1 polymorphisms were detected in this region and the best candidate alters the coding sequence of F55A12.8 , a gene with unknown function in C. elegans. The human ortholog presents a histone acetyltransferase activity. Intriguingly, the N2 allele of F55A12.8 seems to have appeared during the early lab culture of N2 strain before its first freezing. We now try to confirm the effect of this polymorphism on vulva development and to understand its function in the vulva signaling network.