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Neurodegenerative disorders

Axonal traffic jams

Nature Reviews Neuroscience volume 4, pages 856–857 (2003)Cite this article

In the first study, Gunawardena et al. looked at axonal transport in Drosophila. Flies in which the expression of huntingtin had been reduced by tissue-specific RNAi showed accumulation of organelles within larval nerves, which is typical of a deficit in axonal transport. In addition, reduction of huntingtin in the eye caused neurodegeneration in the eyes of adult flies, similar to that caused by overexpression of mutant huntingtin. These results indicate that normal huntingtin might be involved in axonal transport. But similar deficits were produced by expression of a fragment of huntingtin containing the expanded polyglutamine region, pointing towards a toxic gain of function.

Further investigation revealed that the levels of soluble motor proteins in neurons from flies expressing polyglutamine proteins were reduced. Huntingtin is known to interact with huntingtin-associated protein 1 (HAP1), which in turn associates with a component of the axonal transport system, and the authors suggest that the mutant protein might sequester motor proteins. The resulting shortage of motor proteins in the cell could cause the deficits in axonal transport.

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References

ORIGINAL RESEARCH PAPERS

  1. Gunawardena, S. et al. Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ mutants in Drosophila. Neuron 40, 25–40 (2003)

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  2. Szebenyi, G. et al. Neuropathogenic forms of huntingtin and androgen receptor inhibit fast axonal transport. Neuron 40, 41–52 (2003)

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FURTHER READING

  1. Muqit, M. M. K. & Feany, M. B. Modelling neurodegenerative disorders in Drosophila: a fruitful approach? Nature Rev. Neurosci. 3, 237–243 (2002)

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Authors
  1. Rachel Jones
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Jones, R. Axonal traffic jams. Nat Rev Neurosci 4, 856–857 (2003). https://doi.org/10.1038/nrn1268

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  • DOI: https://doi.org/10.1038/nrn1268

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