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Citation
Kahali, B., Bose, A., Karandikar, U., Bishop, C.P., Bidwai, A.P. (2009). On the mechanism underlying the divergent retinal and bristle defects of M8* (E(spl)D) in Drosophila.  genesis 47(7): 456--468.
FlyBase ID
FBrf0208367
Publication Type
Research paper
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 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.

PubMed ID
PubMed Central ID
PMC2777619 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    genesis
    Title
    genesis
    Publication Year
    2000-
    ISBN/ISSN
    1526-954X 1526-968X
    Data From Reference