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Article

Characterization of axonal transport defects in Drosophila Huntingtin mutants.

Journal of neurogenetics - 1 Jan 2000

Weiss Kurt R, Littleton J Troy

Abstract excerpt

Polyglutamine (polyQ) expansion within Huntingtin (Htt) causes the fatal neurodegenerative disorder Huntington's Disease (HD). Although Htt is ubiquitously expressed and conserved from Drosophila to humans, its normal biological function is still being elucidated. Here we characterize a role for the Drosophila Htt homolog (dHtt) in fast axonal transport (FAT). Generation and expression of transgenic dHtt-mRFP and...

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Identifiers

PMID: 27309588
DOI: 10.1080/01677063.2016.1202950
PMCID: PMC5525331

Genes

HAP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Characterization of axonal transport defects in Drosophila Huntingtin mutants.PMID 27309588Read ↗

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Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's disease.Semantic proximity Read ↗

The regulation of autophagosome dynamics by huntingtin and HAP1 is disrupted by expression of mutant huntingtin, leading to defective cargo degradation.Semantic proximity Read ↗

Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's disease.Semantic proximity Read ↗

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