Ras effector switching promotes divergent cell fates in C. elegans vulval patterning. Academic Article uri icon


  • The C. elegans vulva is patterned by epidermal growth factor (EGF) activation of Ras to control 1° fate, and 1° fate induces antagonistic Notch-dependent 2° fate. Furthermore, a spatial EGF gradient, in addition to inducing 1° fate, directly contributes to 2° fate via an unknown pathway. We find that in addition to its canonical effector, Raf, vulval Ras utilizes an exchange factor for the Ral small GTPase (RalGEF), such that Ras-RalGEF-Ral antagonizes Ras-Raf pro-1° fate activity. Consistent with its restricted expression pattern, Ral participates in EGF pro-2° activity. Thus, we have delineated a Ras effector-switching mechanism whereby position within the morphogen gradient dictates that Ras effector usage is switched to RalGEF from Raf to promote 2° instead of 1° fate. Our observations define the utility of Ras effector switching during normal development and may provide a possible mechanistic basis for cell and cancer-type differences in effector dependency and activation.

published proceedings

  • Dev Cell

altmetric score

  • 1.25

author list (cited authors)

  • Zand, T. P., Reiner, D. J., & Der, C. J

citation count

  • 55

complete list of authors

  • Zand, Tanya P||Reiner, David J||Der, Channing J

publication date

  • January 2011