{"database":"bioimages","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Désirée Schatton"],"journal":["The Journal of Cell Biology"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-JCBD-201607019"],"attach_to":["JCB"],"legend":["Immunoblot of whole-liver lysates of E18.5 neonates probed with anti-CLUH antibodies against N-terminal (N) or C-terminal (C) epitopes. Pan-actin was used as loading control.","Representative immunoblots of MEFs grown in glucose (-) or galactose (+) media for 20 h for selected CLUH mRNA target.","CLUH expression in murine tissues at 5 weeks of age.","Immunoblot of WT and KO tissues at E18.5 probed for CLUH.","Representative immunoblot of whole-liver lysates of WT mice at different ages. GAPDH was used as a loading control. L = low exposure, H = high exposure."],"repository":["bioimages"],"figure_sub":["Image 641967 (Figure 1 - E)","Figure 1 - A","Image 641963 (Figure 7 - F)","Figure 1 - E","Image 641968 (Figure 1 - A)","Figure 1 - D","Figure 7 - F","Figure 4","Figure 7","Figure 1","Image 641962 (Figure 4 - D)","Image 641958 (Figure 1 - D)","Figure 4 - D"],"pubmed_authors":["Vidya Velagapudi","Peter Zentis","Teresa Corona","David Pla-Martin","Esther Barth","Arnaud Mourier","Marie-Charlotte Marx","Elena I. Rugarli","Alberto Pessia","Vangelis Kondylis","Astrid C. Schauss","Henriette Hansen","Désirée Schatton","Ivan Nemazanyy"],"additional_accession":[]},"is_claimable":false,"name":"CLUH regulates mitochondrial metabolism by controlling translation and decay of target mRNAs","description":"Mitochondria are essential organelles that host crucial metabolic pathways and produce adenosine triphosphate. The mitochondrial proteome is heterogeneous among tissues and can dynamically change in response to different metabolic conditions. Although the transcriptional programs that govern mitochondrial biogenesis and respiratory function are well known, posttranscriptional regulatory mechanisms remain unclear. In this study, we show that the cytosolic RNA-binding protein clustered mitochondria homologue (CLUH) regulates the expression of a mitochondrial protein network supporting key metabolic programs required under nutrient deprivation. CLUH exerts its function by controlling the stability and translation of target messenger RNAs. In the absence of <jats:italic>Cluh</jats:italic>, mitochondria are severely depleted of crucial enzymes involved in catabolic energy-converting pathways. CLUH preserves oxidative mitochondrial function and glucose homeostasis, thus preventing death at the fetal–neonatal transition. In the adult liver, CLUH ensures maximal respiration capacity and the metabolic response to starvation. Our results shed new light on the posttranscriptional mechanisms controlling the expression of mitochondrial proteins and suggest novel strategies to tailor mitochondrial function to physiological and pathological conditions.","dates":{"release":"2017-02-10T11:29:12Z","modification":"2018-11-29T11:29:12Z","creation":"2018-11-29T11:29:12Z"},"accession":"S-JCBD-201607019","cross_references":{"doi":["10.1083/jcb.201607019"]}}