On the mechanism underlying the divergent retinal and bristle defects of M8* (E(spl)D) in Drosophila
| Autor: | Ashok P. Bidwai, Clifton P. Bishop, Bhaskar Kahali, Umesh C. Karandikar, Anasua Bose |
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| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Genetics
Transgene Neurogenesis Mutant Cell Biology Biology Bristle Article Retina Cell biology Endocrinology Two-Hybrid System Techniques Eye development Phosphorylation Animals Drosophila Proteins Drosophila sense organs Signal transduction Psychological repression Drosophila Protein Signal Transduction |
| Popis: | Our results, using endogenous mutants and Gal4-UAS driven transgenes, implicate multisite phosphorylation in repression by E(spl)M8. We propose that these phosphorylations occur in the morphogenetic furrow (MF) to reverse an auto-inhibited state of M8, enabling repression of Atonal during R8 specification. Our studies address the paradoxical behavior of M8*, the truncated protein encoded by E(spl)D. We suggest that differences in N signaling in the bristle versus the eye underlie the antimorphic activity of M8* in N(+) (ectopic bristles) and hypermorphic activity in N(spl) (reduced eye). Ectopic M8* impairs eye development (in N(spl)) only during establishment of the atonal feedback loop (anterior to the MF), but is ineffective after this time point. In contrast, a CK2 phosphomimetic M8 lacking Groucho (Gro) binding, M8SDDeltaGro, acts antimorphic in N(+) and suppresses the eye/R8 and bristle defects of N(spl), as does reduced dosage of E(spl) or CK2. Multisite phosphorylation could serve as a checkpoint to enable a precise onset of repression, and this is bypassed in M8*. Additional implications are discussed. |
| Databáze: | OpenAIRE |
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