The sensory rays are a set of nine bilateral pairs of peripheral sense organs that extend radially from the tail and that are embedded within a lateral fold of cuticle called the fan. The rays form during the last, or L4, larval stage in a precise pattern within the lateral epidermis (Sulston et al., 1980; Baird et al., 1991). This pattern depends upon the rays expressing unique identities that determine their interactions with the cells of the surrounding epidermis (Baird et al., 1991; Savage et al., 1995).
The copulatory spicules are a pair of needle-like structures made of schlerotic cuticle. They are made by the cells of the proctodeum during the L4 larval stage (Sulston et al., 1980). The proctodeal cells that secrete spicule cuticle also act as molds that determine spicule morphology. The shapes of these cellular molds is determined, in part, by the migrations of two bilateral pairs of cells, B.al/rapapa and B.al/rappv.
The ray and spicule defects observed daf-4 mutant males indcates that TGFb signalling is required for the proper development of these copulatory structures. It also implies that genes with similar mutant phenotypes may encode additional components of TGFb signalling pathways. Three such genes, sma- 2, sma-3, and sma-4, have been identified (GenBank: U34778, U34902, and U34596, respectively)(Baird et al., 1991; Savage et al., 1995). These genes are homologous to eachother and constitute a conserved multigene family, termed the Dwarfin family. Homologues have been identified in mouse, human and Drosophila (Savage et al., 1995; Sekelsky et al., 1995). The Drosophila homologue, mad, was identified as an enhancer of weak decapentaplegic alleles (Sekelsky et al., 1995), a further indication that Dwarfin gene family members of are required for TGFb signalling.
Our current research is focused on the biochemical function of Dwarfin proteins, and on the identification of additional components of TGFb signalling pathways. To address the first problem, we have constructed a sma-4::GFP (green fluorescent protein) reporter gene. Using this reporter gene, fluorescence has been reproducibly observed in two tissues, the body wall musculature and the male-specific musculature. We plan to confirm this localization using antiSMA-4 antibodies.
To address the second problem, we are conducting a variety of genetic screens targeting genes that act downstream of daf-4. These screens are being conducted in collaboration with Marie Sutherlin at the University of Nebraska. Several candidate mutations have been obtained and are being characterized.
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