unc-86 mutants have behavioral defects that are caused by defects in the development or functioning of particular neurons that express the gene. Using the
unc-86/GFP fusion gene to visualize neuronal processes of
unc-86-expressing neurons, we found that their gross neuroanatomy was normal in an
unc-86 null mutant. Thus,
unc-86-regulated gene products may mediate post- pathfinding events in neurogenesis, such as recognition of synaptic partners, synapse formation, or synaptic transmission. We would like to identify the
unc-86 regulated genes that mediate these neurogenic events. Our genetic strategy to identify genes regulated by
unc-86 during neurogenesis uses a hyperactive UNC-86 protein to activate excessive expression of downstream genes. Downstream genes are identified as mutants that suppress phenotypes confered by the hyperactive
unc-86 gene, or as mutants whose phenotypes are suppressed by the hyperactive
unc-86 gene. We activated UNC-86 expressed from its own promoter by fusing it to VP16, a potent transcriptional activator. The
unc-86/VP16 fusion gene is expressed normally, and the fusion gene complements an
unc-86 null mutant for mechanosensation. Strains bearing the
unc-86/VP16 transgene do not express
mec-7 ectopically and the neuroanatomy of the mechanosensory cells is normal. Interestingly, animals habituate to touch much more quickly that normal, but do not respond more robustly. In addition, wild type and
unc-86 mutant animals bearing the
unc-86/VP16 transgene are Egl, Unc, Che, and pharyngeal pumping constitutive, suggesting that the UNC-86/VP16 fusion protein also hyperactivates downstream genes in other neurons that mediate these behaviors. We are testing whether the
unc-86/VP16 fusion gene can suppress weak mutations in
mec-3 and
mec-7, and whether the
unc-86/VP16 phenotypes depend on its ability to bind DNA.