ArticleThe American journal of pathology2014
Silencing of drpr leads to muscle and brain degeneration in adult Drosophila.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Comparative analysis of draper mutant alleles and RNAi expression systems in the ovary and brain of Drosophila melanogaster.G3 (Bethesda, Md.) · 2026Article
- ACSS2 involved in acetyl-CoA synthesis regulates skeletal muscle function.FEBS letters · 2025Article
- Defective phagocytosis leads to neurodegeneration through systemic increased innate immune signaling.iScience · 2023Article
- The Notch signaling pathway in skeletal muscle health and disease.Muscle & nerve · 2022Review
- A secreted factor NimrodB4 promotes the elimination of apoptotic corpses by phagocytes in Drosophila.EMBO reports · 2021Article
- A form of muscular dystrophy associated with pathogenic variants in JAG2.American journal of human genetics · 2021Article
- Megf10 deficiency impairs skeletal muscle stem cell migration and muscle regeneration.FEBS open bio · 2021Article
- Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation.Cell reports · 2020Article
- Social reprogramming in ants induces longevity-associated glia remodeling.Science advances · 2020Article
- MEGF11 is related to tumour recurrence in triple negative breast cancer via chemokine upregulation.Scientific reports · 2020Article
- Planarian EGF repeat-containing genes megf6 and hemicentin are required to restrict the stem cell compartment.PLoS genetics · 2020Article
- Selective serotonin reuptake inhibitors ameliorate MEGF10 myopathy.Human molecular genetics · 2019Article
- Article
- Dying Neurons Utilize Innate Immune Signaling to Prime Glia for Phagocytosis during Development.Developmental cell · 2019Article
- Genetic Architecture of Feeding Behavior and Feed Efficiency in a Duroc Pig Population.Frontiers in genetics · 2018Article
- Glial contributions to neuronal health and disease: new insights from Drosophila.Current opinion in neurobiology · 2017Review
- Consequences of MEGF10 deficiency on myoblast function and Notch1 interactions.Human molecular genetics · 2017Article
- Delayed glial clearance of degenerating axons in aged Drosophila is due to reduced PI3K/Draper activity.Nature communications · 2016Article
- Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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Authors and funding
6 authors.
Funding
Abstract
Mutations in the gene encoding the single transmembrane receptor multiple epidermal growth factor-like domain 10 (MEGF10) cause an autosomal recessive congenital muscle disease in humans. Although mammalian MEGF10 is expressed in the central nervous system as well as in skeletal muscle, patients carrying mutations in MEGF10 do not show symptoms of central nervous system dysfunction. drpr is the sole Drosophila homolog of the human genes MEGF10, MEGF11, and MEGF12 (JEDI, PEAR). The functional domains of MEGF10 and drpr bear striking similarities, and residues affected by MEGF10 mutations in humans are conserved in drpr. Our analysis of drpr mutant flies revealed muscle degeneration with fiber size variability and vacuolization, as well as reduced motor performance, features that have been observed in human MEGF10 myopathy. Vacuolization was also seen in the brain. Tissue-specific RNAi experiments demonstrated that drpr deficiency in muscle, but not in the brain, leads to locomotor defects. The histological and behavioral abnormalities seen in the affected flies set the stage for further studies examining the signaling pathway modulated by MEGF10/Drpr in muscle, as well as assessing the effects of genetic and/or pharmacological manipulations on the observed muscle defects. In addition, the absence of functional redundancy for Drpr in Drosophila may help elucidate whether paralogs of MEGF10 in humans (eg, MEGF11) contribute to maintaining wild-type function in the human brain.
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