ArticleJournal of cell science2016
The effects of ER morphology on synaptic structure and function in Drosophila melanogaster.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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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Who cites it
59 citing papers in PubMed, 91 citations in OpenAlex.
- Endoplasmic Reticulum Geometry Dictates Neuronal Bursting via Calcium Store Refill Rates and Exposes Selective Neuronal Vulnerability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ER discontinuities are common inbioRxiv : the preprint server for biology · 2026Article
- Mitochondrial origins of the pressure to sleep.Nature · 2025Article
- PDZD8 promotes autophagy at ER-lysosome membrane contact sites to regulate activity-dependent synaptic growth.Cell reports · 2025Article
- Loss of Fic causes progressive neurodegeneration in a Drosophila model of hereditary spastic paraplegia.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Atlastin-1 regulates endosomal tubulation and lysosomal proteolysis in human cortical neurons.Neurobiology of disease · 2024Article
- The Drosophila Nesprin-1 homolog MSP300 is required for muscle autophagy and proteostasis.Journal of cell science · 2024Article
- Dissecting the mechanism of atlastin-mediated homotypic membrane fusion at the single-molecule level.Nature communications · 2024Article
- Atl (atlastin) regulates mTor signaling and autophagy in Drosophila muscle through alteration of the lysosomal network.Autophagy · 2024Article
- Article
- Motor neuron activity enhances the proteomic stress caused by autophagy defects in the target muscle.PloS one · 2024Article
- Drosophila Atlastin regulates synaptic vesicle mobilization independent of bone morphogenetic protein signaling.Biological research · 2023Article
- Identification of atlastin genetic modifiers in a model of hereditary spastic paraplegia in Drosophila.Human genetics · 2023Article
- Drosophila SPG12 ortholog, reticulon-like 1, governs presynaptic ER organization and Ca2+ dynamics.The Journal of cell biology · 2023Article
- Decreasing pdzd8-mediated mito-ER contacts improves organismal fitness and mitigates AβLife science alliance · 2022Article
- Dichotomous cis-regulatory motifs mediate the maturation of the neuromuscular junction by retrograde BMP signaling.Nucleic acids research · 2022Article
- Microgravity enhances the phenotype of Arabidopsis zigzag-1 and reduces the Wortmannin-induced vacuole fusion in root cells.NPJ microgravity · 2022Article
- A toolbox to study metabolic status ofSTAR protocols · 2022Article
- The Drosophila melanogaster attP40 docking site and derivatives are insertion mutations of msp-300.PloS one · 2022Article
- The hypervariable region of atlastin-1 is a site for intrinsic and extrinsic regulation.The Journal of cell biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Hereditary spastic paraplegia (HSP) is a set of genetic diseases caused by mutations in one of 72 genes that results in age-dependent corticospinal axon degeneration accompanied by spasticity and paralysis. Two genes implicated in HSPs encode proteins that regulate endoplasmic reticulum (ER) morphology. Atlastin 1 (ATL1, also known as SPG3A) encodes an ER membrane fusion GTPase and reticulon 2 (RTN2, also known as SPG12) helps shape ER tube formation. Here, we use a new fluorescent ER marker to show that the ER within wild-type Drosophila motor nerve terminals forms a network of tubules that is fragmented and made diffuse upon loss of the atlastin 1 ortholog atl. atl or Rtnl1 loss decreases evoked transmitter release and increases arborization. Similar to other HSP proteins, Atl inhibits bone morphogenetic protein (BMP) signaling, and loss of atl causes age-dependent locomotor deficits in adults. These results demonstrate a crucial role for ER in neuronal function, and identify mechanistic links between ER morphology, neuronal function, BMP signaling and adult behavior.
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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.