
Mitochondria in the fat tissue of mice is unable to produce SLC35A4-MP, causing mitochondria to be at risk structurally and functional imbalance. Credit: The Mitochondria Salik Institute in the fat tissue of mice is unable to produce SLC35A4-MP, causing the mitochondria to be at risk structurally and a functional processor. Credit: Salik Institute
Like bees that breathe life in gardens, provide pollen and make flowers flourish, small cellular machines called mitochondria breathe life in our bodies, and they wander with energy because they produce fuel that refers to both cells. Mitochondria metabolism requires inputs from many molecules and proteins – some of which have not been discovered.
The Salik Institute researchers take a closer look on whether the mitochondria depends on the micro proteins – the proteins that were difficult to find, and therefore, it was reduced to its role in health and disease. In their new study, a small protein that was discovered only last year was found in the SALK, called SLC35A4-MP, plays an important role in supporting the structure of mitochondria and organizing metaphorical stress in mouse fat cells. The seed results are planted for the delicate protein of obesity, aging, and other mitochondria disorders.
The study, published in Science progress On August 29, 2025, it is part of a series of modern discoveries in the SALK that presents functional importance of micro proteins in cellular biology, The independenceAnd tension.
“Microbiology has long been rejected as a random genetic scrap, but our work adds to an increasing group of research that shows that many of them are conscience organizers of cell function.” “Here we reveal that the exact protein is responsible for maintaining the structure of mitochondria and the function in brown fat tissue, which regulates the body temperature and the balance of energy.”
In late Spring in 2024, the Saghatelian Laboratory discovered the genetic code for SLC35A4-MP Hidden in the framework of an open -up reading on a strand of Messenger RNA (MRNA). The belief has long been that all symbols of a flexible strand of one protein-one ratio to one from MRNA to protein, always. Therefore, when scientists find additional sections of genetic materials – open reading tires on the source – on flexible threads, they thought they should be either 1) non -informed or organizational symbol that affects the translation of this Marna.
But when the technology of investigation and genetic sequence became more advanced, the researchers soon realized some of the open -coded reading tires of functional proteins. This discovery has brought a completely new dimension to aerated life, as microscopic proteins have long hidden in open reading frames that have been ignored in the direction of the source are now in prosperity – ready to benefit and study it.
Some first functional functional proteins have been involved in metabolism and the regulation of mitochondria. This includes the Saghatelian 2024 study, where the laboratory was first discovered SLC35A4-MP in the walls of mitochondria. Additional tests indicated that exact protein may help maintain healthy cell metabolism.

Ripe fat cells in mice show SLC34a4-MP (red), DNA (blue), and mitochondria (green). Credit: Salik Institute
However, these results were based on the data collected from biochemical stimulants in the test tubes and cells cultivated in Petri dishes. To confirm the description of the entire physiological role of the SLC35A4-MP, they will have to test its function in the living system.
“SLC35A4-MP is among the first accurate proteins that are prescribed functional in mice,” says the first author Andrea Rocha, post-PhD researcher at the Sajabian Laboratory. “In fact, we found that SLC35A4-MP regulates the function of mitochondria and the metabolism of fats in mice, which really shows that microscopic proteins cannot be overlooked while searching for biological factors that regulate health.”
For the SLC35A4-MP classification, researchers looked at ideal metabolic tissue working in the mitochondria in particular: brown fat. The meal fat cells require metabolic, as they regulate energy balance and body temperature. The researchers have completely removed SLC35a4-MP from mouse brown fat cells, then caused by stressful events such as cold exposure or a high-fat diet.
Without SLC35A4-MP, mice were unable to seek metabolism during cold exposure. Their mitochondria was at risk structurally, expanding, dysfunction, and inflamed. Outside the mitochondria, other parts of brown fat cells were also affected. The researchers saw signs of internal cells and additional inflammation-signs of declining metabolism in obesity-related conditions.
The results show the basic role played by SLC35A4-MP in regulating the function of brown fat cells and responding to metaphorical stress. Because mitochondria, loud cell bees are found in every type of cell in the body, the results extend every place as well. SLC35A4-MP can be a strong therapeutic target for any disease or disorder that affects metabolism and mitochondria, from obesity to aging and outside.
Deficient protein research emerges in life, and the team sees bright flowers in the search for more functional micro proteins.
“Since scientists have managed to add more precision proteins to our protein databases, the question has remained, does these micro proteins have any physiological connection?” Sghaphelian says. “Our study says yes, they are important physiological organizers. I hope it adds more fuel to the study of micro proteins that move forward.”
Peno Dedrich, Shan. The Christian Research Foundation Guy Perksin and Mark Eleasman from the University of California in San Diego; Plucińska and Paul Cohen of Rockefar University; UC said from Diego.
More information:
Andréa L. Rocha et al, unnatural mitochondria structure and function in the brown fat tissue of the sliced mice SLC35A4-MP, Science progress (2025). Two: 10.1126/Sciaadv.Ads7381
quoteResearchers discover the new precise protein that controls metabolic health in mouse lipid cells (2025, August 30) on August 31, 2025 of https://phys.org/news
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