Researchers from the Institute for Research in Biomedicine (IRB) and from the universities of Barcelona (Spain) and Padua (Italy) have discovered two variants of the same proteinMitofusin 2, which are vital because their interaction maintains optimal cell function.
The research, published in the journal Science, has revealed the key role of cellular Mitofusin 2 in the interconnection of organelles within cells, where mitochondria depend on intricate connections for fluid communication.
Among these organelles, the mitochondria (known as cellular power plants) and the endoplasmic reticulum (responsible for protein and lipid synthesis) maintain vital exchanges, explained IRB researcher Antonio Zorzano, co-director of the study.
Research has discovered the existence of different “variants” of the Mitofusin 2 protein, called ERMIT2 and ERMIN2, which are generated through ‘alternative splicing’, a process in which segments of the gene called “exons” they rearrange to generate different proteins from the same DNA sequence.
What has surprised the researchers is that ERMIN2 and ERMIT2, two hitherto unknown variants derived from the mitochondrial protein Mitofusin 2, do not localize in the mitochondria themselves, but in the endoplasmic reticulum.
“Our research found ERMIN2 and ERMIT2 in a wide range of human cells and tissues, including adipose tissue, muscle, and liver, and has revealed the role of these proteins in maintaining optimal cellular functionality.” summarized Zorzano, leader of the laboratory of Complex Metabolic Diseases and Mitochondria at the IRB in Barcelona.
“This study represents one of the few cases in which these alternative variants of mitochondrial proteins have been observed. Consequently, the interaction and mechanism of action that we describe in this study are highly innovative.”highlighted the researcher Deborah Naón, who started the project during her doctoral studies at the IRB in Barcelona and continued it during her postdoctoral stage at VIMM and the University of Padua.
The discovery has already allowed Zorzano’s team to improve liver function in models of non-alcoholic steatohepatitis simply by stimulating the production of the ERMIT2 bridging protein.
“The interaction between mitochondria and the endoplasmic reticulum is also altered in syndromes that present insulin resistance, such as diabetes and obesity. Therefore, this finding presents a potential therapeutic strategy that is worth exploring.”pointed out Zorzano, who is also a professor of Biology at the University of Barcelona (UB) and a member of CIBERDEM.
Zorzano recalled that mutations in the Mitofusin 2 gene cause Charcot-Marie-Tooth 2A disease, a genetic peripheral neuropathy characterized by severe muscle weakness in the legs that ends up placing patients in wheelchairs.
“The discovery of ERMIN2 and ERMIT2 opens the possibility that alterations in the endoplasmic reticulum and the communication of this organelle with mitochondria contribute to the clinical manifestations of this disease. If so, we could explore new therapeutic strategies specific to this currently intractable disorder.” according to the researchers.
Source: EFE
Source: Gestion
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