High impact information on vab-1

• Nematodes mutated in dog-1 showed germline as well as somatic deletions in genes containing polyguanine tracts, such as vab-1 [1].
• In the absence of VAB-1 signaling, ephrin-expressing neurons are disorganized. vab-2/efn-1 mutations synergize with vab-1 kinase alleles, suggesting that VAB-2/EFN-1 may partly function in a kinase-independent VAB-1 pathway [2].
• Mutations in the C. elegans vab-1 gene disrupt the coordinated movements of cells during two periods of embryogenesis. vab-1 mutants are defective in the movement of neuroblasts during closure of the ventral gastrulation cleft and in the movements of epidermal cells during ventral enclosure of the embryo by the epidermis [3].
• We show that vab-1 encodes a receptor tyrosine kinase of the Eph family [3].
• A double-mutant combination between vab-1 and slt-1 unmasks a role for the SLT-1 ligand in embryogenesis [4].

Biological context of vab-1

• The genetic interaction of vab-1 and ptp-3 suggests that LAR-like RPTPs and Eph receptors have related and partly redundant functions in C. elegans morphogenesis [5].
• The predominant axonal defect in vab-1 mutant animals was an overextension axon phenotype [6].

References