¿regulación de la vía de señalización de torso en el desarrollo temprano de drosophila melanogaster¿

Resumo

Development of terminal structures in Drosophila embryo is controlled by Torso receptor tyrosine kinase (RTK). As other maternal genes, torso is expressed in the nurse cell during oogenesis, the mRNA is dumped into the oocyte, and its translation is activated after fecundation. The Torso receptor, ubiquitously localized on the embryo surface, is activated only in the polar regions by a localized processing of its ligand, trunk. We identified a new element involved in Drosophila terminal patterning, named rumpf (rum). Embryos lied from rum homozygous females show phenotypes resembling those of Torso lack of function. We show that rum is a new allele of pipsqueak (psq), a large and complex locus, which, through the use of alternative promoters and alternative splicing, gives rise to at least 12 different transcripts, encoding two different classes of proteins. Psq has been described as a transcription factor affecting various processes, from oogenesis to eye development, through epigenetic silencing of different genes. Here we propose a new role for psq as a transcriptional regulator of Torso: in psqrum mutant ovaries, torso transcription is strongly reduced, leading to an insufficient amount of dumped mRNA. Furthermore we show that torso is the only affected element of the pathway, since other mRNAs are expressed at normal levels in mutants and expression of UAS-torso rescues the rum phenotype. Our results indicate a specific transcriptional effect of Pipsqueak on torso expression, suggesting a strict and individual control of maternal gene expression. On the other hand, Torso has been recently reported to trigger pupariation, acting as the receptor of a differend ligand, named PTTH, in a different tissue, the prothoracic gland. torso mutants and RNAis show significant pupariation delay. Using antibody staining, in situ hybridization and lacZ reporters, we show that torso-like, a gene which seem to be essential for the correct processing of Trunk, is expressed in the prothoracic gland. Different combinations of Tsl alleles give developmental delay and overgrowth, similar to what has been observed for torso mutants. On the other hand, other genes that act upstream of Torso in the early embryo don¿t seem to be required for Torso activity in the prothoracic gland. Since Torso-like seem to be required for Trunk processing/activation, we propose a model in which the same machinery could be involved in the activation of PTTH.