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Background  Teneurins are transmembrane proteins that assist morphogenetic processes in many organisms.  ten-1  is the  C. elegans  teneurin homolog with two transcripts,  ten-1a  and  ten-1b , that respectively encode a long (TEN-1L) and short (TEN-1S) form of the protein. We previously isolated a  C. elegans  mutant where one pharyngeal neuron was frequently misplaced, and now show that it corresponds to a novel allele of  ten-1 .    Results  The novel  ten-1(et5)  allele is a hypomorph since its post-embryonic phenotype is weaker than the null alleles  ten-1(ok641)  and  ten-1(tm651) .  ten-1  mutants have defects in all pharyngeal neurons that we examined, and in vivo reporters show that only the long form of the  ten-1  gene is expressed in the pharynx, specifically in six marginal cells and the M2 neurons. Defects in the pharyngeal M2 neurons were enhanced when the  ten-1(ok641)  mutation was combined with mutations in the following genes:  mig-14 ,  unc-5, unc-51, unc-52  and  unc-129 . None of the body neurons examined show any defects in the  ten-1(ok641)  mutant, but genetic interaction studies reveal that  ten-1(ok641)  is synthetic lethal with  sax-3, unc-34  and  unc-73 , and examination of the hypodermal cells in embryos of the  ten-1(ok641)  mutant point to a role of  ten-1  during hypodermal cell morphogenesis.    Conclusions  Our results are consistent with  ten-1  normally providing a function complementary to the cytoskeletal remodeling processes that occur in migrating cells or cells undergoing morphogenesis. It is possible that  ten-1  influences the composition/distribution of extracellular matrix.

C. elegans ten-1 is synthetic lethal with mutations in cytoskeleton regulators, and enhances many axon guidance defective mutants