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Research Paper
Altered Expression of the Noncoding hsrω Gene Enhances poly-Q Induced Neurotoxicity in Drosophila
Sonali Sengupta and S.C. Lakhotia
volume 3 | issue 1
january/february/march 2006Pages: 28 - 35
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In an earlier report two P-transposon insertion alleles of the noncoding hsrω gene, hsrω05241 and P292 were shown to enhance neurodegeneration caused by expression of ataxin-1 protein with expanded poly-Q in a Drosophila model. In present study, we examined the possible relation between hsrω gene expression and toxicity due to poly-Q pathogenesis. The Drosophila hsrω gene produces several noncoding transcripts in almost all cell types, of which the >10 kb long hsr?-n transcript organizes heterogeneous RNA binding (hnRNPs) and related proteins as nucleoplasmic omega speckles. We show that P insertion alleles of the hsrω gene, which cause its overexpression, dominantly enhance neurodegeneration in fly eyes expressing either expanded poly-Q (127Q) or mutant huntingtin protein. Null allele of Hrb87F gene, encoding hnRNPA1, and a novel gene’s mutant allele (l(3)pl10R), which affects the omega speckles, also dominantly enhance 127Q-induced neurodegeneration. The hsrω-n transcripts or the hnRNPs do not colocalize with the poly-Q nuclear inclusion bodies, neither in hsrω wild type, nor in hsrω mutant background. However, the levels of poly-Q and Hsp70 were significantly higher in hsrω mutant eye discs. Sequestration of hnRNPs and other related RNA-binding proteins by overexpression of hsrω transcripts in hsrω05241 or in l(3)pl10R background or the reduced levels of Hrb87F protein seem to affect nuclear RNA metabolism, thus enhancing the toxicity due to poly-Q expansion.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.