ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
dAcsl, the Drosophila ortholog of acyl-CoA synthetase long-chain family member 3 and 4, inhibits synapse growth by attenuating bone morphogenetic protein signaling via endocytic recycling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Modeling AP2M1 developmental and epileptic encephalopathy in Drosophila.Disease models & mechanisms · 2025Article
- Upregulation of ACSL, ND75, Vha26 and sesB genes by antiepileptic drugs resulted in genotoxicity in drosophila.Toxicology research · 2024Article
- Review
- Inter-Species Rescue of Mutant Phenotype-The Standard for Genetic Analysis of Human Genetic Disorders inInternational journal of molecular sciences · 2022Review
- An update on the therapeutic implications of long-chain acyl-coenzyme A synthetases in nervous system diseases.Frontiers in neuroscience · 2022Review
- ACSL4 as a Potential Target and Biomarker for Anticancer: From Molecular Mechanisms to Clinical Therapeutics.Frontiers in pharmacology · 2022Review
- Cell death inhibitors protect against brain damage caused by cardiac ischemia/reperfusion injury.Cell death discovery · 2021Article
- Immunohistochemical staining reveals differential expression of ACSL3 and ACSL4 in hepatocellular carcinoma and hepatic gastrointestinal metastases.Bioscience reports · 2020Article
- Rosy Beginnings: Studying Peroxisomes inFrontiers in cell and developmental biology · 2020Review
- Target-dependent retrograde signaling mediates synaptic plasticity at the Drosophila neuromuscular junction.Developmental neurobiology · 2019Article
- Targeting Long Chain Acyl-CoA Synthetases for Cancer Therapy.International journal of molecular sciences · 2019Review
- The endogenous subcellular localisations of the long chain fatty acid-activating enzymes ACSL3 and ACSL4 in sarcoma and breast cancer cells.Molecular and cellular biochemistry · 2018Article
- The glycosphingolipid MacCer promotes synaptic bouton formation in Drosophila by interacting with Wnt.eLife · 2018Article
- Neuroligin 4 regulates synaptic growth via the bone morphogenetic protein (BMP) signaling pathway at theThe Journal of biological chemistry · 2017Article
- MAN1 Restricts BMP Signaling During Synaptic Growth in Drosophila.Cellular and molecular neurobiology · 2017Article
- Down-regulation of coasy, the gene associated with NBIA-VI, reduces Bmp signaling, perturbs dorso-ventral patterning and alters neuronal development in zebrafish.Scientific reports · 2016Article
- Scribbled Optimizes BMP Signaling through Its Receptor Internalization to the Rab5 Endosome and Promote Robust Epithelial Morphogenesis.PLoS genetics · 2016Article
- Role of BMP receptor traffic in synaptic growth defects in an ALS model.Molecular biology of the cell · 2016Article
- Article
- Drosophila S6 Kinase like inhibits neuromuscular junction growth by downregulating the BMP receptor thickveins.PLoS genetics · 2015Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatty acid metabolism plays an important role in brain development and function. Mutations in acyl-CoA synthetase long-chain family member 4 (ACSL4), which converts long-chain fatty acids to acyl-CoAs, result in nonsyndromic X-linked mental retardation. ACSL4 is highly expressed in the hippocampus, a structure critical for learning and memory. However, the underlying mechanism by which mutations of ACSL4 lead to mental retardation remains poorly understood. We report here that dAcsl, the Drosophila ortholog of ACSL4 and ACSL3, inhibits synaptic growth by attenuating BMP signaling, a major growth-promoting pathway at neuromuscular junction (NMJ) synapses. Specifically, dAcsl mutants exhibited NMJ overgrowth that was suppressed by reducing the doses of the BMP pathway components, accompanied by increased levels of activated BMP receptor Thickveins (Tkv) and phosphorylated mothers against decapentaplegic (Mad), the effector of the BMP signaling at NMJ terminals. In addition, Rab11, a small GTPase involved in endosomal recycling, was mislocalized in dAcsl mutant NMJs, and the membrane association of Rab11 was reduced in dAcsl mutant brains. Consistently, the BMP receptor Tkv accumulated in early endosomes but reduced in recycling endosomes in dAcsl mutant NMJs. dAcsl was also required for the recycling of photoreceptor rhodopsin in the eyes, implying a general role for dAcsl in regulating endocytic recycling of membrane receptors. Importantly, expression of human ACSL4 rescued the endocytic trafficking and NMJ phenotypes of dAcsl mutants. Together, our results reveal a novel mechanism whereby dAcsl facilitates Rab11-dependent receptor recycling and provide insights into the pathogenesis of ACSL4-related mental retardation.
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Registered trials
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.