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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Expanded polyglutamine protein forms nuclear inclusions and causes neural degeneration in Drosophila.

Spinocerebellar ataxia type 3 (SCA3/ MJD) is one of at least eight human neurodegenerative diseases caused by glutamine-repeat expansion. We have recreated glutamine-repeat disease in Drosophila using a segment of the SCA3/ MJD protein. Targeted expression of the protein with an expanded polyglutamine repeat led to nuclear inclusion (NI) formation and late-onset cell degeneration. Differential sensitivity to the mutant transgene was observed among different cell types, with neurons being particularly susceptible; NI formation alone was not sufficient for degeneration. The viral antiapoptotic gene P35 mitigated polyglutamine-induced degeneration in vivo. Our results demonstrate that cellular mechanisms of human glutamine-repeat disease are conserved in invertebrates. This fly model will aid in identifying additional factors that modulate neurodegeneration.[1]

References

  1. Expanded polyglutamine protein forms nuclear inclusions and causes neural degeneration in Drosophila. Warrick, J.M., Paulson, H.L., Gray-Board, G.L., Bui, Q.T., Fischbeck, K.H., Pittman, R.N., Bonini, N.M. Cell (1998) [Pubmed]
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