A group of researchers at Karolinska Institutet and the Max Planck Institute for Biology of Ageing has discovered that a protein called MTERF4 combines with another protein called NSUN4 to form a complex that controls the formation and function of the mitochondrial ribosomes. In mice lacking MTERF4 no functional ribosomes are formed, leading to a reduction in energy production.
“Reduced mitochondrial function is involved in several inherited diseases, normal ageing and age-related diseases,” says Professor Nils Göran Larsson, who co-led the study with Professor Claes Gustafsson. “Fundamental knowledge of how mitochondrial function is regulated can therefore be of great clinical significance in the future.”
The research group previously discovered similar regulation mechanisms in the mitochondria that were found to be related to the development of diabetes.
Publication:
Yolanda Cámara, Jorge Asin-Cayuela, Chan Bae Park, Metodi D. Metodiev, Yonghong Shi, Benedetta Ruzzenente, Christian Kukat, Bianca Habermann; Rolf Wibom, Kjell Hultenby, Thomas Franz, Hediye Erdjument-Bromage, Paul Tempst, B. Martin Hallberg, Claes M. Gustafsson & Nils-Göran Larsson
MTERF4 regulates translation by targeting the methyltransferase NSUN4 to the mammalian mitochondrial ribosome
Cell Metabolism, online 3 May 2011
