Abstract

This presentation presents three newly identified genes, involved in migration of the two distal tip cells (DTC"s) of the somatic gonad of Caenorhabditis elegans, forming a characteristic bilobed and U-formed structure. The hermaphroditic gonad develops in a developmental process in three phases. Phase 1: the two DTC"s migrate anterior and posterior along the ventral body muscle band away from the midbody, the migratory origin. Phase 2: Reorientation of the migrating DTC in a strictly dorsal direction. Phase 3: Reorientation and backward migration to the midbody along dorsal muscle band. The last two parts of gonad migration happens during the third larval stage. Events of that stage are regulated by heterochronic genes, mainly by daf-12. Some mutants in daf-12 fail to undergo specific stage specific programs, including phase two and three of gonad development leading to a completely linear gonad. I present evidence, that pcp-2, pcp-3 and gon-12 also act at that part of gonad development. pcp-2 and pcp-3 encode carboxypeptidases, which might take part in a multienzyme complex. gon-12 is a new mutation and is allelic to unc-129, which encodes a TGFb. That gene regulates with UNC-5 and UNC-6/Netrin late migration of the DTC within a physiological dorsoventral polarity. Depending on morphological differtial states at the third larval stage, dauer larva or reproductively growing L3 larva, pcp-2, pcp-3 and gon-12 also affect adult vulval morphology, being recognised by a huge protrusion, a phenotype, which has been named Ppv for "pseudovulval protrusion". In the gon-12 mutant the phenotype is caused by an earlier proliferation of the six vulval precursor cells (VPC"s) leading to a mistake in the further development. But in the case of recovery of the dauer stage, six new VPC"s are determined from that pool of the earlier divided cells and undergo vulval differentiation. In that case the mistake is reversed and a wildtype vulva is formed. The action of pcp-2 and pcp-3 on vulval development is indirect, because after knocking down these genes a normal vulva is formed. But the vulva protrudes after some days of adult life time, depending on dauer stage within their individual life history. The gut protrudes through that wound. That effect corresponds most probable to deranged metabolic control after exit of the dauer stage. It seems obvious, that loss of activity of these carboxypeptidases in the multienzymatic complex results in missing catabolism of substrates in the gut. The protrusion at the vulva is therefore a late consequence.

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