PuSH - Publication Server of Helmholtz Zentrum München

Wredenberg, A.* ; Lagouge, M.* ; Bratic, A.* ; Metodiev, M.D.* ; Spåhr, H.* ; Mourier, A.* ; Freyer, C.* ; Ruzzenente, B.* ; Tain, L.* ; Grönke, S.* ; Baggio, F.* ; Kukat, C.* ; Kremmer, E. ; Wibom, R.* ; Polosa, P.L.* ; Habermann, B.* ; Partridge, L.* ; Park, C.B.* ; Larsson, N.G.*

MTERF3 regulates mitochondrial ribosome biogenesis in invertebrates and mammals.

PLoS Genet. 9:e1003178 (2013)
Publ. Version/Full Text Volltext DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Regulation of mitochondrial DNA (mtDNA) expression is critical for the control of oxidative phosphorylation in response to physiological demand, and this regulation is often impaired in disease and aging. We have previously shown that mitochondrial transcription termination factor 3 (MTERF3) is a key regulator that represses mtDNA transcription in the mouse, but its molecular mode of action has remained elusive. Based on the hypothesis that key regulatory mechanisms for mtDNA expression are conserved in metazoans, we analyzed Mterf3 knockout and knockdown flies. We demonstrate here that decreased expression of MTERF3 not only leads to activation of mtDNA transcription, but also impairs assembly of the large mitochondrial ribosomal subunit. This novel function of MTERF3 in mitochondrial ribosomal biogenesis is conserved in the mouse, thus we identify a novel and unexpected role for MTERF3 in coordinating the crosstalk between transcription and translation for the regulation of mammalian mtDNA gene expression.
Altmetric
Additional Metrics?
[➜Log in]
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 1553-7390
e-ISSN 1553-7404
Journal PLoS Genetics
Quellenangaben Volume: 9, Issue: 1, Pages: , Article Number: e1003178 Supplement: ,
Publisher Public Library of Science (PLoS)
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Molecular Immunology (IMI)