ArticleCirculation research2010
Gene deletion screen for cardiomyopathy in adult Drosophila identifies a new notch ligand.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
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- MicroRNA-150 Deletion from Adult Myofibroblasts Augments Maladaptive Cardiac Remodeling Following Chronic Myocardial Infarction.Biomolecules · 2024Article
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- A Notch-dependent transcriptional mechanism controls expression of temporal patterning factors ineLife · 2022Article
- LY450139 Inhibited Ti-Particle-Induced Bone Dissolution via Suppressing Notch and NF-κB Signaling Pathways.Calcified tissue international · 2022Article
- MiR-150 Attenuates Maladaptive Cardiac Remodeling Mediated by Long Noncoding RNA MIAT and Directly Represses ProfibroticCirculation. Heart failure · 2022Article
- Comparative transcriptome analyses of the Drosophila pupal eye.G3 (Bethesda, Md.) · 2021Article
- Dissecting Motor Neuron Disease WithFrontiers in neuroscience · 2019Review
- Genetic Modifiers of Neurodegeneration in aGenetics · 2018Article
- β-arrestin-biased agonism of β-adrenergic receptor regulates Dicer-mediated microRNA maturation to promote cardioprotective signaling.Journal of molecular and cellular cardiology · 2018Article
- TheDisease models & mechanisms · 2018Article
- A carvedilol-responsive microRNA, miR-125b-5p protects the heart from acute myocardial infarction by repressing pro-apoptotic bak1 and klf13 in cardiomyocytes.Journal of molecular and cellular cardiology · 2018Article
- A modifier screen identifiesJCI insight · 2016Article
- Carvedilol-responsive microRNAs, miR-199a-3p and -214 protect cardiomyocytes from simulated ischemia-reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2016Article
- Drosophila tools and assays for the study of human diseases.Disease models & mechanisms · 2016Review
- Review
- Identification of gene signatures regulated by carvedilol in mouse heart.Physiological genomics · 2015Article
- Methods to assess Drosophila heart development, function and aging.Methods (San Diego, Calif.) · 2014Review
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3 authors.
Funding
Abstract
rationaleDrosophila has been recognized as a model to study human cardiac diseases.
objectiveDespite these findings, and the wealth of tools that are available to the fly community, forward genetic screens for adult heart phenotypes have been rarely performed because of the difficulty in accurately measuring cardiac function in adult Drosophila. METHODS AND
resultsUsing optical coherence tomography to obtain real-time analysis of cardiac function in awake Drosophila, we performed a genomic deficiency screen in adult flies. Based on multiple complementary approaches, we identified CG31665 as a novel gene causing dilated cardiomyopathy. CG31665, which we name weary (wry), has structural similarities to members of the Notch family. Using cell aggregation assays and gamma-secretase inhibitors we show that Wry is a novel Notch ligand that can mediate cellular adhesion with Notch expressing cells and transactivates Notch to promote signaling and nuclear transcription. Importantly, Wry lacks a DSL (Delta-Serrate-Lag) domain that is common feature to the other Drosophila Notch ligands. We further show that Notch signaling is critically important for the maintenance of normal heart function of the adult fly.
conclusionsIn conclusion, we identify a previously unknown Notch ligand in Drosophila that when deleted causes cardiomyopathy. Our study suggests that Notch signaling components may be a therapeutic target for dilated cardiomyopathy.
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