| Drosophila nemo was initially identified as a tissue polarity gene, with a role in controlling the rotation of the ommatidia in the developing compound eye. More recently, it has emerged as having a role in both Wnt/Wg signaling and TGF-β signaling in C. elegans, Drosophila and vertebrates. Nemo-like kinases act as links between the two pathways, responding to signals from (TGF-β Activated Kinase-1) TAK-1 and modulating the activation of the Wnt/Wg pathway.; The original mutation in nemo, nmoP, was characterized as a null allele, both genetically and by Northern analyses. Novel mutations subsequently generated in our lab (nmoadk1 and nmoadk2) have been shown to exhibit more severe defects than nmoP, including ectopic wing veins and embryonic phenotypes, but still express transcripts, albeit of altered size.; In order to address this incongruity, I generated new alleles of nmo (nmoDB24, nmoDB67, nmo DB71, and nmoDB126) through the excision of the P transposable element in nmoP to confirm disruption of the nmo locus is responsible for the more severe phenotypes of nmoadk1 and nmo adk2. I also analyzed the various nmo alleles molecularly to characterize the nature of the lesions causing the mutant phenotypes. (Abstract shortened by UMI.)... |
