ArticlePloS one2013
The EGF repeat-specific O-GlcNAc-transferase Eogt interacts with notch signaling and pyrimidine metabolism pathways in Drosophila.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
- Intron Retention as a Homeostatic State Variable for Drug Response and Recovery: Lessons from Depression for Broader Applications.International journal of molecular sciences · 2026Review
- Crystal structure of epidermal growth factor domain-specificPNAS nexus · 2026Article
- Crosstalk between O-GlcNAcylation and phosphorylation in metabolism: regulation and mechanism.Cell death and differentiation · 2025Review
- Synergistic regulation of Notch signaling by different O-glycans promotes hematopoiesis.Frontiers in immunology · 2023Article
- Glycans that regulate Notch signaling in the intestine.Biochemical Society transactions · 2022Review
- Significant Roles of NotchMolecules (Basel, Switzerland) · 2022Review
- Role of Notch2 pathway in mature B cell malignancies.Frontiers in oncology · 2022Review
- Structure, function, and pathology of protein O-glucosyltransferases.Cell death & disease · 2021Review
- Multifaceted regulation of Notch signaling by glycosylation.Glycobiology · 2021Review
- RNAi-Mediated Silencing of Pgants Shows Core 1Frontiers in physiology · 2021Article
- Cell Communications among Microorganisms, Plants, and Animals: Origin, Evolution, and Interplays.International journal of molecular sciences · 2020Review
- Synthesis and biological roles of O-glycans in insects.Glycoconjugate journal · 2020Review
- Decoding the PTM-switchboard of Notch.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice.Open biology · 2019Article
- A modifier in the 129S2/SvPasCrl genome is responsible for the viability of Notch1[12f/12f] mice.BMC developmental biology · 2019Article
- O-Linked glycosylation in Drosophila melanogaster.Current opinion in structural biology · 2019Review
- A mouse model for functional dissection of TAB1 O-GlcNAcylation.Wellcome open research · 2019Article
- Multiple roles for O-glycans in Notch signalling.FEBS letters · 2018Review
- Structural Divergence inMolecules (Basel, Switzerland) · 2018Article
- Integration of Drosophila and Human Genetics to Understand Notch Signaling Related Diseases.Advances in experimental medicine and biology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The O-GlcNAc transferase Eogt modifies EGF repeats in proteins that transit the secretory pathway, including Dumpy and Notch. In this paper, we show that the Notch ligands Delta and Serrate are also substrates of Eogt, that mutation of a putative UDP-GlcNAc binding DXD motif greatly reduces enzyme activity, and that Eogt and the cytoplasmic O-GlcNAc transferase Ogt have distinct substrates in Drosophila larvae. Loss of Eogt is larval lethal and disrupts Dumpy functions, but does not obviously perturb Notch signaling. To identify novel genetic interactions with eogt, we investigated dominant modification of wing blister formation caused by knock-down of eogt. Unexpectedly, heterozygosity for several members of the canonical Notch signaling pathway suppressed wing blister formation. And importantly, extensive genetic interactions with mutants in pyrimidine metabolism were identified. Removal of pyrimidine synthesis alleles suppressed wing blister formation, while removal of uracil catabolism alleles was synthetic lethal with eogt knock-down. Therefore, Eogt may regulate protein functions by O-GlcNAc modification of their EGF repeats, and cellular metabolism by affecting pyrimidine synthesis and catabolism. We propose that eogt knock-down in the wing leads to metabolic and signaling perturbations that increase cytosolic uracil levels, thereby causing wing blister formation.
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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.