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• W2014737999 abstract "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 Nspl (reduced eye). Ectopic M8* impairs eye development (in Nspl) 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, M8SDΔGro, acts antimorphic in N+ and suppresses the eye/R8 and bristle defects of Nspl, 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. genesis 47:456–468, 2009. © 2009 Wiley-Liss, Inc." @default.
• W2014737999 created "2016-06-24" @default.
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• W2014737999 date "2009-07-01" @default.
• W2014737999 modified "2023-10-16" @default.
• W2014737999 title "On the mechanism underlying the divergent retinal and bristle defects of M8* (<i>E(spl)D</i>) in Drosophila" @default.
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• W2014737999 doi "https://doi.org/10.1002/dvg.20521" @default.
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