Expression of activated Ras1 partially rescues mesodermal defects associated with htl perturbation (Beiman et al. 1996; Gisselbrecht et al. 1996; Michelson et al. 1998b; Schulz and Gajewski 1999). Ras1 functions downstream or parallel to the adaptor protein Stumps (Carmena et al. 1998; Michelson et al. 1998a; Vincent et al. 1998; Imam et al. 1999) to transduce signals downstream from Htl (Johnson Hamlet and Perkins 2001; Petit et al. 2004; Csiszar et al. 2010). Ectopic expression of activated Aop, a transcriptional repressor downstream from ERK, generates phenotypes similar to that due to htl disruption whereas expression of activated Pnt, a transcriptional activator downstream from ERK, increases the number of somatic muscle progenitors (Halfon et al. 2000). These observations are consistent with Htl-dependent ERK activation (Gabay et al. 1997; Wilson et al. 2004).
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Breathless signaling in the tracheal system. Btl autophosphorylation, on Bnl binding, recruits the adaptor protein Stumps and additional downstream effectors. Ras activation initiates a phosphorylation cascade that culminates in the stimulation of ERK kinase activity. ERK-dependent phosphorylation of the transcriptional activators Grh and Pnt, and the transcriptional repressors Gro and Aop, modulates their activity at promoters. The consequential up-regulation of gene expression induces tracheal cell migration and tracheal branching and fine-tuning of Btl signaling.
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