Practice question

Constitutively active LIN-12 results from gain-of-function mutation deleting extracellular domain, making receptor ligand-independent. Normally LIN-12 Notch restricts primary fate via lateral signaling, promoting secondary fate in P5.p and P7.p. When all VPCs express activated LIN-12, Ras-MAPK mediated primary program blocked by LIN-12 targets lip-1 phosphatase that dephosphorylates MAPK, and lst inhibitors. Consequently even P6.p high LIN-3 cannot sustain primary, all P3.p-P8.p express secondary vulval markers and generate secondary lineages producing symmetrical vulval structures without central primary invagination. This phenotype parallels LIN-12 dominant mutants described by Greenwald showing all secondary fate adoption.