We have investigated the relationship between the function of the gene (), which is the Drosophila homolog of (), and the EGFR signaling pathway. We report that mutant embryos are defective in EGFR signaling dependent processes, namely chordotonal organ recruitment and oenocyte specification. We also show the temperature sensitive hypomorphic allele is enhanced by the hypomorphic MAPK allele ( ). We find that overexpression results in ectopic expression within the embryonic peripheral nervous system, and we show that this effect is EGFR-dependent. Finally, we show that the canonical U-shaped embryonic lethal phenotype of , which is associated with premature degeneration of the extraembyonic amnioserosa and a failure in germ band retraction, is rescued by expression of several components of the EGFR signaling pathway (, , ) as well as the caspase inhibitor Based on this collection of corroborating evidence, we suggest that an overarching function of involves the positive regulation of EGFR signaling.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6945037 | PMC |
http://dx.doi.org/10.1534/g3.119.400829 | DOI Listing |
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