ArticleGenesis (New York, N.Y. : 2000)2009
On the mechanism underlying the divergent retinal and bristle defects of M8* (E(spl)D) in Drosophila.
Article in Genesis (New York, N.Y. : 2000), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Protein kinase CK2 phosphorylates a conserved motif in the Notch effector E(spl)-Mγ.Molecular and cellular biochemistry · 2023Article
- Article
- Control of Neural Daughter Cell Proliferation by Multi-level Notch/Su(H)/E(spl)-HLH Signaling.PLoS genetics · 2016Article
- The Conserved MAPK Site in E(spl)-M8, an Effector of Drosophila Notch Signaling, Controls Repressor Activity during Eye Development.PloS one · 2016Article
- Article
- New insights into the Orange domain of E(spl)-M8, and the roles of the C-terminal domain in autoinhibition and Groucho recruitment.Molecular and cellular biochemistry · 2011Article
- Functional dissection of Timekeeper (Tik) implicates opposite roles for CK2 and PP2A during Drosophila neurogenesis.Genesis (New York, N.Y. : 2000) · 2009Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.