@article{Hasson:2013fk,
	Abstract = {An increasing body of evidence points to mitochondrial dysfunction as a contributor to the molecular pathogenesis of neurodegenerative diseases such as Parkinson's. Recent studies of the PD-associated genes PINK1 and Parkin suggest that they may act in a quality control pathway preventing the accumulation of dysfunctional mitochondria. Here we elucidate regulators impacting Parkin translocation to damaged mitochondria with genome-wide siRNA screens coupled to high-content microscopy. Screening yielded gene candidates involved in diverse cellular processes that were subsequently validated in confirmatory assays. This led to characterization of TOMM7, as essential for stabilizing Pink1 on the outer mitochondrial membrane following mitochondrial damage. Additionally, we discovered HSPA1L (HSP70 family member) and BAG4 play mutually opposing roles in the regulation of Parkin translocation. The screens also revealed that SIAH3, found to localize to mitochondria, inhibits Pink1 accumulation after mitochondrial insult, reducing Parkin translocation. Overall, our screens provide a rich resource to understand mitochondrial quality control.},
	Author = {Hasson, S. and Kane, L. and Sliter, D. and Hessa, T. and Wang, C. and Buehler, E. and Guha, R. and Martin, S. and Yamano, K. and Huang, C.H. and Heman-Ackah, S. and Youle, R.},
	Date-Added = {2013-10-10 02:39:17 +0000},
	Date-Modified = {2014-01-10 00:50:44 +0000},
	Journal = {Nature},
	Pages = {291--295},
	Title = {Genome-wide high-content {RNAi} screens identify regulators of {P}arkin upstream of mitophagy},
	Volume = {504},
	Year = {2013},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature12748}}

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Here we elucidate regulators impacting Parkin translocation to damaged mitochondria with genome-wide siRNA screens coupled to high-content microscopy. Screening yielded gene candidates involved in diverse cellular processes that were subsequently validated in confirmatory assays. This led to characterization of TOMM7, as essential for stabilizing Pink1 on the outer mitochondrial membrane following mitochondrial damage. Additionally, we discovered HSPA1L (HSP70 family member) and BAG4 play mutually opposing roles in the regulation of Parkin translocation. The screens also revealed that SIAH3, found to localize to mitochondria, inhibits Pink1 accumulation after mitochondrial insult, reducing Parkin translocation. Overall, our screens provide a rich resource to understand mitochondrial quality control.","author":[{"propositions":[],"lastnames":["Hasson"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Kane"],"firstnames":["L."],"suffixes":[]},{"propositions":[],"lastnames":["Sliter"],"firstnames":["D."],"suffixes":[]},{"propositions":[],"lastnames":["Hessa"],"firstnames":["T."],"suffixes":[]},{"propositions":[],"lastnames":["Wang"],"firstnames":["C."],"suffixes":[]},{"propositions":[],"lastnames":["Buehler"],"firstnames":["E."],"suffixes":[]},{"propositions":[],"lastnames":["Guha"],"firstnames":["R."],"suffixes":[]},{"propositions":[],"lastnames":["Martin"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Yamano"],"firstnames":["K."],"suffixes":[]},{"propositions":[],"lastnames":["Huang"],"firstnames":["C.H."],"suffixes":[]},{"propositions":[],"lastnames":["Heman-Ackah"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Youle"],"firstnames":["R."],"suffixes":[]}],"date-added":"2013-10-10 02:39:17 +0000","date-modified":"2014-01-10 00:50:44 +0000","journal":"Nature","pages":"291--295","title":"Genome-wide high-content RNAi screens identify regulators of Parkin upstream of mitophagy","volume":"504","year":"2013","bdsk-url-1":"http://dx.doi.org/10.1038/nature12748","bibtex":"@article{Hasson:2013fk,\n\tAbstract = {An increasing body of evidence points to mitochondrial dysfunction as a contributor to the molecular pathogenesis of neurodegenerative diseases such as Parkinson's. Recent studies of the PD-associated genes PINK1 and Parkin suggest that they may act in a quality control pathway preventing the accumulation of dysfunctional mitochondria. Here we elucidate regulators impacting Parkin translocation to damaged mitochondria with genome-wide siRNA screens coupled to high-content microscopy. Screening yielded gene candidates involved in diverse cellular processes that were subsequently validated in confirmatory assays. This led to characterization of TOMM7, as essential for stabilizing Pink1 on the outer mitochondrial membrane following mitochondrial damage. Additionally, we discovered HSPA1L (HSP70 family member) and BAG4 play mutually opposing roles in the regulation of Parkin translocation. The screens also revealed that SIAH3, found to localize to mitochondria, inhibits Pink1 accumulation after mitochondrial insult, reducing Parkin translocation. 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