Tag: Tory Herman

Connections between nerve cells are established by the outgrowth of long projections called “axons.” The motile end of a growing axon is the growth cone, a dynamic structure of actin filaments and microtubules. We are interested in how neurons downregulate the motility of their growth cones once the latter have reached their final targets. Studying this process may improve our under standing of how neurons control growth cone motility during regeneration after injury. In the Drosophila eye, R7 photoreceptor neurons are born in the retina of the fly and project their axons into the optic lobe. The Herman lab has found that the transcription factor Tramtrack69 (Ttk69) is required to prevent R7 axons from continuing to grow even after they reach their targets. Ttk69 is absent from R7s during axon outgrowth but present in R7s as their axons approach their targets. Early misexpression of Ttk69 causes premature termination of R7 axons. We conclude that Ttk69 is both necessary and sufficient to restrict axonal growth. We have found that Ttk69 does so by promoting signaling through the conserved TGF/Activin pathway. Because Ttk69 is known to be a transcriptional repressor, we hypothesize that Ttk69 represses an antagonist of the Activin pathway. Using RNA interference, I will disrupt expression of genes known to antagonize Activin signaling, including follistatin and cripto-like, in R7 cells lacking Ttk69. Suppression of the ttk69 mutant phenotype would indicate that the gene in question might be a target of Ttk69 repression.