ArticleMolecular and cellular biology2007
Regulation of Commissureless by the ubiquitin ligase DNedd4 is required for neuromuscular synaptogenesis in Drosophila melanogaster.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Ubiquitin ligase signalling networks shape presynaptic development, function and disease.The Journal of physiology · 2025Review
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- Different temporal requirements for tartan and wingless in the formation of contractile interfaces at compartmental boundaries.Development (Cambridge, England) · 2022Article
- Article
- The Ubiquitinated Axon: Local Control of Axon Development and Function by Ubiquitin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- The Ubiquitin Proteasome System in Neuromuscular Disorders: Moving Beyond Movement.International journal of molecular sciences · 2020Review
- The deubiquitinase USP6 affects memory and synaptic plasticity through modulating NMDA receptor stability.PLoS biology · 2019Article
- Regulation of SH3PX1 by dNedd4-long at theThe Journal of biological chemistry · 2019Article
- The WAGR syndrome gene PRRG4 is a functional homologue of the commissureless axon guidance gene.PLoS genetics · 2017Article
- Intestinal knockout of Nedd4 enhances growth of ApcOncogene · 2016Article
- Drosophila Nedd4-long reduces Amphiphysin levels in muscles and leads to impaired T-tubule formation.Molecular biology of the cell · 2016Article
- Control of the dynamics and homeostasis of the Drosophila Hedgehog receptor Patched by two C2-WW-HECT-E3 Ubiquitin ligases.Open biology · 2015Article
- The role of ubiquitin-mediated pathways in regulating synaptic development, axonal degeneration and regeneration: insights from fly and worm.The Journal of physiology · 2013Review
- Commissureless regulation of axon outgrowth across the midline is independent of Rab function.PloS one · 2013Article
- Septin 4, the drosophila ortholog of human CDCrel-1, accumulates in parkin mutant brains and is functionally related to the Nedd4 E3 ubiquitin ligase.Journal of molecular neuroscience : MN · 2012Article
- Ubiquitin-dependent endocytosis, trafficking and turnover of neuronal membrane proteins.Molecular and cellular neurosciences · 2012Review
- The ubiquitin ligase Nedd4-1 participates in denervation-induced skeletal muscle atrophy in mice.PloS one · 2012Article
- A splice isoform of DNedd4, DNedd4-long, negatively regulates neuromuscular synaptogenesis and viability in Drosophila.PloS one · 2011Article
- The ubiquitin ligase Nedd4-1 is required for heart development and is a suppressor of thrombospondin-1.The Journal of biological chemistry · 2010Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Muscle synaptogenesis in Drosophila melanogaster requires endocytosis of Commissureless (Comm), a binding partner for the ubiquitin ligase dNedd4. We investigated whether dNedd4 and ubiquitination mediate this process. Here we show that Comm is expressed in intracellular vesicles in the muscle, whereas Comm bearing mutations in the two PY motifs (L/PPXY) responsible for dNedd4 binding [Comm(2PY-->AY)], or bearing Lys-->Arg mutations in all Lys residues that serve as ubiquitin acceptor sites [Comm(10K-->R)], localize to the muscle surface, suggesting they cannot endocytose. Accordingly, aberrant muscle innervation is observed in the Comm(2PY-->AY) and Comm(10K-->R) mutants expressed early in muscle development. Similar muscle surface accumulation of Comm and innervation defects are observed when dNedd4 is knocked down by double-stranded RNA interference in the muscle, in dNedd4 heterozygote larvae, or in muscles overexpressing catalytically inactive dNedd4. Expression of the Comm mutants fused to a single ubiquitin that cannot be polyubiquitinated and mimics monoubiquitination [Comm(2PY-->AY)-monoUb or Comm(10K-->R)-monoUb] prevents the defects in both Comm endocytosis and synaptogenesis, suggesting that monoubiquitination is sufficient for Comm endocytosis in muscles. Expression of the Comm mutants later in muscle development, after synaptic innervation, has no effect. These results demonstrate that dNedd4 and ubiquitination are required for Commissureless endocytosis and proper neuromuscular synaptogenesis.
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