title: HuR controls mitochondrial morphology through the regulation of BclxLtranslation.
abstract: BclxLis a key prosurvival factor that in addition to controlling mitochondrial membrane permeability regulates mitochondrial network dynamics. The expression of BclxLis regulated at the level of translation, splicing and selective translation. In this study, we show that the RNA-binding protein HuR, which is known to orchestrate an anti-apoptotic cellular program, functions as a translational repressor of BclxL. We show that HuR binds directly to the 5'UTR of BclxL, and represses BclxLtranslation through the inhibition of its internal ribosome entry site (IRES). Reduction of HuR levels leads to the derepression of BclxLtranslation and subsequent rearrangement of the mitochondrial network. Our results place BclxLinto the HuR-regulated operon and provide further insight into the regulation of cellular stress response by HuR.
authors.affiliation: Apoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute.
authors.forename: Danielle
authors.initials: D
authors.lastname: Durie
authors.affiliation: Department of Nutrition, Case Western Reserve University, School of Medicine, Cleveland, Ohio, U.S.A.
authors.forename: Maria
authors.initials: M
authors.lastname: Hatzoglou
authors.affiliation: Department of Pediatrics, University of Ottawa ; Newborn Screening Ontario, Children's Hospital of Eastern Ontario, 401 Smyth Road, Ottawa, K1H 8L1, Canada.
authors.forename: Pranesh
authors.initials: P
authors.lastname: Chakraborty
authors.affiliation: Apoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute ; Department of Pediatrics, University of Ottawa.
authors.forename: Martin
authors.initials: M
authors.lastname: Holcik
keywords: IRES; ITAF; RNA binding protein; mitochondrial dynamics; translational control