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Comments on Cumbo, Philip et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Regulation of cell fate specification by Wnt signaling in the nematodes C. elegans and C. briggsae" (0)
Overview
Cumbo, Philip, Seetharaman, Ashwin, Bojanala, Nagagireesh, Thillainathan, Bavithra, & Gupta, Bhagwati (2010). Regulation of cell fate specification by Wnt signaling in the nematodes C. elegans and C. briggsae presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.
The C. elegans vulva is an established model system to understand how genes and pathways function to control organ formation. The study of vulval development has been crucial to identifying the components of conserved signaling pathways, such as Wnt, and dissecting their mechanism of function. The canonical Wnt signaling pathway has been extensively studied in C. elegans and components that play a pivotal role in vulva development have been identified. We are interested in understanding the role of Wnt signaling in other nematode species and its evolutionary differences from C. elegans . To facilitate this we are focusing on Wnt pathway genes in C. briggsae , a sister species of C. elegans . By taking a forward genetics approach we isolated Cbr-pry-1 (Axin homolog) mutants that display multiple pseudo-vulvae resulting from ectopic VPC induction. The pry-1 phenotype in C. briggsae and C. elegans was characterized through genetic interactions with Wnt pathway components. We also used molecular markers to identify the fates of induced VPCs. From this analysis we can conclude that ectopically induced VPCs adopt a 2 0 cell fate independent of the LIN-12/Notch lateral signal, which indicates that activated Wnt signaling is able to confer a specific cell fate on vulval precursors. Interestingly, P7.p frequently fails to be induced in Cbr-pry-1 mutants, which is also observed in Cel-pry-1 mutants, but to a lesser degree. Further characterization of this particular defect was shown to be caused by altered LIN-12/Notch signaling through persistent lip-1 (MAPK) expression. To understand how Wnt signaling regulates these processes we are currently screening for Cbr-pry-1 suppressor mutations. The findings of these experiments will be discussed with regards to both C. elegans and C. briggsae vulval development.