NAR Breakthrough: Dynamic interplay between RPL3- and RPL3L-containing ribosomes modulates mitochondrial activity in the mammalian heart
NAR Nucleic Acids Research
Published by Oxford University Press - Impact Factor 16.7
by Ivan Milenkovic, Helaine Graziele Santos Vieira, Morghan C Lucas, Jorge Ruiz-Orera, Giannino Patone, Scott Kesteven, Jianxin Wu, Michael Feneley, Guadalupe Espadas, Eduard Sabidó, Norbert Hübner, Sebastiaan van Heesch, Mirko V?lkers, Eva Maria Novoa
Ribosomes are macromolecular machines responsible for protein synthesis in all living beings. Recent studies have shown that ribosomes can be heterogeneous in their structure, possibly leading to a specialized function. Here, we focus on RPL3L, a ribosomal protein expressed exclusively in striated muscles. We find that the deletion of the Rpl3l gene in a mouse model triggers a compensation mechanism, in which the missing RPL3L protein is replaced by its paralog, RPL3. Furthermore, we find that RPL3-containing ribosomes establish closer interactions with mitochondria, cellular organelles responsible for energy production, leading to higher energy production when compared to RPL3L-containing ribosomes. Finally, we show that the RPL3-RPL3L compensation mechanism is also triggered in heart disease conditions, such as hypertrophy and myocardial infarction.