ArticleNature neuroscience2011
Drosophila Rae1 controls the abundance of the ubiquitin ligase Highwire in post-mitotic neurons.
Article in Nature neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Synaptic Cell Adhesion: A Functional Perspective.Advances in neurobiology · 2026Review
- PDZD8 promotes autophagy at ER-lysosome membrane contact sites to regulate activity-dependent synaptic growth.Cell reports · 2025Article
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- The response of Dual-leucine zipper kinase (DLK) to nocodazole: Evidence for a homeostatic cytoskeletal repair mechanism.PloS one · 2024Article
- The circular RNA Edis regulates neurodevelopment and innate immunity.PLoS genetics · 2022Article
- Autophagy in axonal and presynaptic development.Current opinion in neurobiology · 2021Review
- Autophagy is inhibited by ubiquitin ligase activity in the nervous system.Nature communications · 2019Article
- Genome-Wide Association Study of Circadian Behavior in Drosophila melanogaster.Behavior genetics · 2019Article
- BMP signaling downstream of the Highwire E3 ligase sensitizes nociceptors.PLoS genetics · 2018Article
- Drosophila Studies on Autism Spectrum Disorders.Neuroscience bulletin · 2017Review
- Defining Minimal Binding Regions in Regulator of Presynaptic Morphology 1 (RPM-1) UsingThe Journal of biological chemistry · 2017Article
- Models of axon regeneration in Drosophila.Experimental neurology · 2017Review
- The Hippo Pathway Targets Rae1 to Regulate Mitosis and Organ Size and to Feed Back to Regulate Upstream Components Merlin, Hippo, and Warts.PLoS genetics · 2016Article
- Angelman Syndrome Protein Ube3a Regulates Synaptic Growth and Endocytosis by Inhibiting BMP Signaling in Drosophila.PLoS genetics · 2016Article
- The PHR proteins: intracellular signaling hubs in neuronal development and axon degeneration.Neural development · 2016Review
- Developmental Function of the PHR Protein RPM-1 Is Required for Learning in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2015Article
- Transmission, Development, and Plasticity of Synapses.Genetics · 2015Review
- Autophagy in synaptic development, function, and pathology.Neuroscience bulletin · 2015Review
- Mask loss-of-function rescues mitochondrial impairment and muscle degeneration of Drosophila pink1 and parkin mutants.Human molecular genetics · 2015Article
- The RanGTP Pathway: From Nucleo-Cytoplasmic Transport to Spindle Assembly and Beyond.Frontiers in cell and developmental biology · 2015Review
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5 authors at 2 institutions in 1 country.
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Abstract
The evolutionarily conserved Highwire (Hiw)/Drosophila Fsn E3 ubiquitin ligase complex is required for normal synaptic morphology during development and axonal regeneration after injury. However, little is known about the molecular mechanisms that regulate the Hiw E3 ligase complex. Using tandem affinity purification techniques, we identified Drosophila Rae1 as a previously unknown component of the Hiw/Fsn complex. Loss of Rae1 function in neurons results in morphological defects at the neuromuscular junction that are similar to those seen in hiw mutants. We found that Rae1 physically and genetically interacts with Hiw and restrains synaptic terminal growth by regulating the MAP kinase kinase kinase Wallenda. Moreover, we found that the Rae1 is both necessary and sufficient to promote Hiw protein abundance, and it does so by binding to Hiw and protecting Hiw from autophagy-mediated degradation. These results describe a previously unknown mechanism that selectively controls Hiw protein abundance during synaptic development.
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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.