Effects of kinesin mutations on neuronal functions
Open accessAbstract
Kinesin is believed to generate force for the movement of organelles in anterograde axonal transport. The identification of genes that encode kinesin-like proteins suggests that other motors may provide anterograde force instead of or in addition to kinesin. To gain insight into the specific functions of kinesin, the effects of mutations in the kinesin heavy chain gene (khc) on the physiology and ultrastructure of Drosophila larval neurons were studied. Mutations in khc impair both action potential propagation in axons and neurotransmitter release at nerve terminals but have no apparent effect on the concentration of synaptic vesicles in nerve terminal cytoplasm. Thus kinesin is required in vivo for normal neuronal function and may be active in the transport of ion channels and components of the synaptic release machinery to their appropriate cellular locations. Kinesin appears not to be required for the anterograde transport of synaptic vesicles or their components.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Kinesin-I plays a primary role in neuronal transport.
“Previous studies with mutants lacking KHC in invertebrate organisms have all given neuronal phenotypes (Saxton et al. 1991; Gho et al. 1992; Patel et al. 1993; Hurd and Saxton 1996), suggesting that kinesin-I plays a primary role in neuronal transport.”
From Defective kinesin heavy chain behavior in mouse kinesin light chain mutants (1999) · cites this paper as Gho et al. 1992
Kinesin is required for axonal transport in neuronal cells.
“Genetic studies in Caenorhabditis elegans, Drosophila melanogaster, and mice have failed to identify the primary cargo of conventional kinesin although, they have demonstrated that kinesin is required for axonal transport in neuronal cells (Saxton et al. 1991; Gho et al. 1992; Patel et al. 1993; Hurd and Saxton 1996; Hurd et al. 1996; Gindhart et al. 1998; Tanaka et al. 1998; Rahman et al. 1999).”
From Cargo of kinesin identified as JIP scaffolding proteins and associated signaling molecules (2001) · cites this paper as Gho et al. 1992
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 22 · Cited by 120
- Authors
- Gho, M., McDonald, K., Ganetzky, B., & Saxton, W. M.
- Affiliations
- University of Wisconsin–Madison (US)
- University of Colorado Boulder (US)
- Indiana University Bloomington (US)
- ORCID
- Venue
- Science
- Published
- 1992-10-09
- Volume
- 258
- Issue
- 5080
- Pages
- 313-316
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3203545
- OpenAlex
- W2062535587
- Cited by
- 120
- References
- 22
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2019: 1 · 2017: 2 · 2015: 1 · 2014: 4 · 2013: 1 · 2012: 4
- FWCI
- 5.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM046295)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- kinesin, kinesin heavy chain, anterograde axonal transport, action potential propagation, neurotransmitter release, synaptic vesicles, ion channel transport, neuronal ultrastructure
- MeSH terms
- Action Potentials, Animals, Axons, Cytoplasm, Drosophila, Evoked Potentials, Ion Channels, Larva, Microscopy, Electron, Motor Neurons, Nerve Endings, Synapses, Synaptic Vesicles, Mutagenesis, Kinesins, Neurotransmitter Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
