ArticleGenetics2011
Loss of Drosophila melanogaster p21-activated kinase 3 suppresses defects in synapse structure and function caused by spastin mutations.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Deciphering the Impact of AKT1 Pathogenic Variants in Juvenile Granulosa Cell Tumors Using a Drosophila Model.Molecular & cellular proteomics : MCP · 2025Article
- Wings of Discovery: UsingCells · 2025Review
- Cul-4 inhibition rescues spastin levels and reduces defects in hereditary spastic paraplegia models.Brain : a journal of neurology · 2024Article
- Inhibition of negative feedback for persistent epithelial cell-cell junction contraction by p21-activated kinase 3.Nature communications · 2022Article
- Suppression ofFrontiers in neuroscience · 2020Article
- Glial response to hypoxia in mutants of NPAS1/3 homolog Trachealess through Wg signaling to modulate synaptic bouton organization.PLoS genetics · 2019Article
- MCTP is an ER-resident calcium sensor that stabilizes synaptic transmission and homeostatic plasticity.eLife · 2017Article
- The effects of ER morphology on synaptic structure and function in Drosophila melanogaster.Journal of cell science · 2016Article
- The Presynaptic Microtubule Cytoskeleton in Physiological and Pathological Conditions: Lessons from Drosophila Fragile X Syndrome and Hereditary Spastic Paraplegias.Frontiers in molecular neuroscience · 2016Review
- Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia.Molecular neurodegeneration · 2015Review
- A Critical Role of GIT1 in Vertebrate and Invertebrate Brain Development.Experimental neurobiology · 2015Article
- Cold temperature improves mobility and survival in Drosophila models of autosomal-dominant hereditary spastic paraplegia (AD-HSP).Disease models & mechanisms · 2014Article
- Group I PAKs function downstream of Rac to promote podosome invasion during myoblast fusion in vivo.The Journal of cell biology · 2012Article
- PAK family kinases: Physiological roles and regulation.Cellular logistics · 2012Article
- Development and plasticity of the Drosophila larval neuromuscular junction.Wiley interdisciplinary reviews. Developmental biologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Microtubules are dynamic structures that must elongate, disassemble, and be cleaved into smaller pieces for proper neuronal development and function. The AAA ATPase Spastin severs microtubules along their lengths and is thought to regulate the balance between long, stable filaments and shorter fragments that seed extension or are transported. In both Drosophila and humans, loss of Spastin function results in reduction of synaptic connections and disabling motor defects. To gain insight into how spastin is regulated, we screened the Drosophila melanogaster genome for deletions that modify a spastin overexpression phenotype, eye size reduction. One suppressor region deleted p21-activated kinase 3 (pak3), which encodes a member of the Pak family of actin-regulatory enzymes, but whose in vivo function is unknown. We show that pak3 mutants have only mild synaptic defects at the larval neuromuscular junction, but exhibit a potent genetic interaction with spastin mutations. Aberrant bouton morphology, microtubule distribution, and synaptic transmission caused by spastin loss of function are all restored to wild type when pak3 is simultaneously reduced. Neuronal overexpression of pak3 induces actin-rich thin projections, suggesting that it functions in vivo to promote filopodia during presynaptic terminal arborization. pak3 therefore regulates synapse development in vivo, and when mutated, suppresses the synaptic defects that result from spastin loss.
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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.