Practice question

LIN-12 encodes Notch family transmembrane receptor regulating temporal, somatic gonad, and vulval fates through lateral signaling feedback. Gain-of-function alleles cause constitutive Notch intracellular domain signaling independent of LAG-2 ligand due to missense in extracellular EGF repeats or intracellular PEST degradation domain. In VPCs, ectopic LIN-12 drives excessive secondary fate adoption, antagonizing MAPK primary induction feedback leading to multiple ventral invaginations or multivulva phenotype with extra pseudovulvae expressing 2° markers. Conversely, loss yields two anchor cells, demonstrating dosage sensitivity of Notch balancing 1° versus 2° outcomes.