Torso-like influences developmental timing in Drosophila melanogaster independently of the Torso RTK pathway. Travis K. Johnson^1,2, Tova Crossman², Karyn Foote², Michelle A. Bennett², Lauren Forbes Beadle², Anabel Herr^1,2, James C. Whisstock¹, Coral G. Warr². 1) Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, 3800, Australia; 2) School of Biological Sciences, Monash University, Clayton, Victoria, 3800, Australia.

   Membrane attack complex/perforin-like (MACPF) proteins are best known for their ability to lyse and kill target cells during the vertebrate immune response, however several MACPF proteins play poorly understood roles in development. The Drosophila MACPF protein Torso-like (Tsl) is critical for terminal patterning in the early embryo and restricts activation of the Torso (Tor) receptor tyrosine kinase by an unknown mechanism. Recently, Tor was shown to have a second role in the prothoracic gland (PG), as the receptor for prothoracicotropic hormone (Ptth), which initiates metamorphosis¹. Here, we explored the possibility that tsl and other terminal patterning genes might also be required for this process. We looked for expression of known maternal terminal class genes (tsl, trunk, fs(1)Nasrat, fs(1)polehole and closca) in the PG and found only tsl is expressed here. To test if tsl participates in Tor signalling in the PG, we generated tsl null mutants via ends-out gene replacement. tsl nulls phenocopied loss of tor exhibiting a delay in the time to pupariation, and this was rescued by expression of a tsl transgene. However, in tsl; tor double mutants the delay was greatly increased when compared to loss of tor or tsl alone, suggesting the effect of loss of tsl is additive rather than epistatic to loss of tor. Furthermore, we found that ectopic Ptth was highly active in both the PG and the embryo independently of tsl, producing faster development and an expansion of terminal regions respectively. Taken together we conclude that tsl is acting independently of Ptth/Tor in the PG to influence developmental timing. 1. Rewitz et al. (2009) Science 326, 1403-1405.