| Literature DB >> 28864412 |
Ju Zheng1, Junsheng Yang2, Young-Jun Choe3, Xinxin Hao2, Xiuling Cao2, Qian Zhao4, Yuejie Zhang4, Vanessa Franssens5, F Ulrich Hartl3, Thomas Nyström2, Joris Winderickx5, Beidong Liu6.
Abstract
The subcellular localization of polyQ-expanded huntingtin exon1 (Httex1) modulates polyQ toxicity in models of Huntington's disease. Using genome-wide screens in a yeast model system, we report that the ribosome quality control (RQC) machinery, recently implicated in neurodegeneration, is a key determinant for the nucleocytoplasmic distribution of Httex1-103Q. Deletion of the RQC genes, LTN1 or RQC1, caused the accumulation of Httex1-103Q in the nucleus through a process that required the CAT-tail tagging activity of Rqc2 and transport via the nuclear pore complex. We provide evidence that nuclear accumulation of Httex1-103Q enhances its cytotoxicity, suggesting that the RQC machinery plays an important role in protecting cells against the adverse effects of polyQ expansion proteins.Entities:
Keywords: Huntington's disease; Nucleocytoplasmic translocation; PolyQ protein; RQC
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Year: 2017 PMID: 28864412 DOI: 10.1016/j.bbrc.2017.08.126
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575