Reference Report

Reference
Citation	Bodai, L., Pallos, J., Thompson, L.M., Marsh, J.L. (2012). Pcaf Modulates Polyglutamine Pathology in a Drosophila Model of Huntington's Disease. Neurodegener. Dis. 9(2): 104--106. (Export to RIS)
FlyBase ID	FBrf0217401
Publication Type	Research paper
PubMed ID	21912091
PubMed Abstract	Huntingtin peptides with elongated polyglutamine domains, the root causes of Huntington's disease, hinder histone acetylation, which leads to transcriptional dysregulation. However, the range of acetyltransferases interacting with mutant Huntingtin has not been systematically evaluated. We used genetic interaction tests in Drosophila to determine whether specific acetyltransferases belonging to distinct protein families influence polyglutamine pathology. We found that flies expressing a mutant form of the Huntingtin protein (Httex1pQ93) exhibit reduced viability, which is further decreased by partial loss of Pcaf or nejire, while the tested MYST family acetyltransferases did not affect pathology. Reduced levels of Pcaf also led to the increased degeneration of photoreceptor neurons in the retina. Overexpression of Pcaf, however, was not sufficient to ameliorate these phenotypes, and the level of soluble Pcaf is unchanged in Httex1pQ93-expressing flies. Thus, our results indicate that while Pcaf has a significant impact on Huntington's disease pathology, therapeutic strategies aimed at elevating its levels are likely to be ineffective in ameliorating Huntington's disease pathology; however, strategies that aim to increase the specific activity of Pcaf remain to be tested.
DOI	10.1159/000330505
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Language of Publication	English
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Parent Publication
Publication Type	Journal
Abbreviation	Neurodegener. Dis.
Title	Neuro-degenerative Diseases
Publication Year	2004-
ISBN/ISSN	1660-2854 1660-2862
Data from Reference
Aberrations (2)
	Df(3L)iro-2 Df(3R)Exel6259
Alleles (7)
	enok² Gcn5^E333st Gcn5^Scer\UAS.cBa Hsap\HTT^{Q93.ex1p.Scer\UAS} mof² nej³ Scer\GAL4^elav-C155
Constructs (2)
	P{UAS-HTT.Q93.ex1p} P{UAS-Pcaf.B}
Genes (7)
	CG1894 enok Gcn5 Hsap\HTT mof nej Scer\GAL4
Insertions (1)
	P{GawB}elav^C155
Natural transposons (1)
	P-element