ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Importin-beta11 regulates synaptic phosphorylated mothers against decapentaplegic, and thereby influences synaptic development and function at the Drosophila neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 42 citations in OpenAlex.
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- Tissue-specific I-Smad mechanisms revealed by structure-function analysis inLife science alliance · 2026Article
- Elucidation of the binding interaction interface between AAV serotype 11 capsid protein and host nuclear import proteins.Molecular therapy. Methods & clinical development · 2025Article
- RNA profiling of sEV (small extracellular vesicles)/exosomes reveals biomarkers and vascular endothelial dysplasia with moyamoya disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- γ-secretase promotes Drosophila postsynaptic development through the cleavage of a Wnt receptor.Developmental cell · 2022Article
- BMP/TGF-β signaling as a modulator of neurodegeneration in ALS.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Importin-9 regulates chromosome segregation and packaging in Drosophila germ cells.Journal of cell science · 2021Article
- A Conserved Role for Vezatin Proteins in Cargo-Specific Regulation of Retrograde Axonal Transport.Genetics · 2020Article
- Importin-11 is Essential for Normal Embryonic Development in Mice.International journal of medical sciences · 2020Article
- Target-dependent retrograde signaling mediates synaptic plasticity at the Drosophila neuromuscular junction.Developmental neurobiology · 2019Article
- Pathogenic Huntington Alters BMP Signaling and Synaptic Growth through Local Disruptions of Endosomal Compartments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Role of BMP receptor traffic in synaptic growth defects in an ALS model.Molecular biology of the cell · 2016Article
- A Novel, Noncanonical BMP Pathway Modulates Synapse Maturation at the Drosophila Neuromuscular Junction.PLoS genetics · 2016Article
- An Importin Code in neuronal transport from synapse-to-nucleus?Frontiers in molecular neuroscience · 2015Article
- Prodomain removal enables neto to stabilize glutamate receptors at the Drosophila neuromuscular junction.PLoS genetics · 2015Article
- Differential centrifugation-based biochemical fractionation of the Drosophila adult CNS.Nature protocols · 2014Article
- Gene expression changes in spinal motoneurons of the SOD1(G93A) transgenic model for ALS after treatment with G-CSF.Frontiers in cellular neuroscience · 2014Article
- Axon-soma communication in neuronal injury.Nature reviews. Neuroscience · 2014Review
- Postsynaptic glutamate receptors regulate local BMP signaling at the Drosophila neuromuscular junction.Development (Cambridge, England) · 2014Article
- Epsin 1 Promotes Synaptic Growth by Enhancing BMP Signal Levels in Motoneuron Nuclei.PloS one · 2013Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Importin proteins act both at the nuclear pore to promote substrate entry and in the cytosol during signal trafficking. Here, we describe mutations in the Drosophila gene importin-beta11, which has not previously been analyzed genetically. Mutants of importin-beta11 died as late pupae from neuronal defects, and neuronal importin-beta11 was present not only at nuclear pores but also in the cytosol and at synapses. Neurons lacking importin-beta11 were viable and properly differentiated but exhibited discrete defects. Synaptic transmission was defective in adult photoreceptors and at larval neuromuscular junctions (NMJs). Mutant photoreceptor axons formed grossly normal projections and synaptic terminals in the brain, but synaptic arbors on larval muscles were smaller while still containing appropriate synaptic components. Bone morphogenic protein (BMP) signaling was the apparent cause of the observed NMJ defects. Importin-beta11 interacted genetically with the BMP pathway, and at mutant synaptic boutons, a key component of this pathway, phosphorylated mothers against decapentaplegic (pMAD), was reduced. Neuronal expression of an importin-beta11 transgene rescued this phenotype as well as the other observed neuromuscular phenotypes. Despite the loss of synaptic pMAD, pMAD persisted in motor neuron nuclei, suggesting a specific impairment in the local function of pMAD. Restoring levels of pMAD to mutant terminals via expression of constitutively active type I BMP receptors or by reducing retrograde transport in motor neurons also restored synaptic strength and morphology. Thus, importin-beta11 function interacts with the BMP pathway to regulate a pool of pMAD that must be present at the presynapse for its proper development and function.
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