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Understanding how the process begins can point to new directions in the study of aging – ScienceDaily

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Many age-related diseases have one thing in common: cell mitochondria begin to function. Although the reason is unknown, scientists at the Buck Institute have discovered a new mechanism for how mitochondria begin to go wrong, which opens new doors for researchers to learn how to start solving the problem.

“Now that we have a different hypothesis about why mitochondrial dysfunction occurs during aging and age-related diseases, we are discovering a completely different way to think about, measure, mitigate and reverse the process,” said Dr. Chuankai (Kai). ) Zhou. , who is the senior author of a study published in the March 2 issue eLifea leading journal on biomedical research, created by the Howard Hughes Medical Institute, the Max Planck Society, and the Wellcome Trust.

Mitochondria are commonly referred to as the “powerhouse” of a cell because bean-like structures provide the units of energy needed by each cell to function. They are involved in many important processes including immune response, inflammation and metabolism.

According to Zhou, mitochondrial dysfunction is associated with most chronic diseases, including neurodegenerative disorders, cardiovascular disease, cancer, diabetes and obesity. More and more evidence shows that this dysfunction contributes to aging in general.

The Zhou team wanted to study the contribution of “mitochondrial biogenesis” to mitochondrial dysfunction during aging. Mitochondrial biogenesis is a cellular process that produces new mitochondria. It determines both the quality and quantity of mitochondria in cells that shrink during normal aging. Over the past couple of decades, scientists have described two major stages of mitochondrial biogenesis: activation of mitochondrial protein transcription in the cell nucleus in response to nutrient / metabolic signals and import of these newly synthesized mitochondrial proteins from the cytozole into the cytozole. However, it was unclear how these two stages of mitochondrial biogenesis coordinated with each other to streamline the synthesis and import of mitochondrial proteins. Zhou’s team found that a conserved receptor molecule on the mitochondrial surface called Tom70 may be responsible for coordinating these two steps by regulating the transcriptional activity of mitochondrial proteins in the nucleus.

It was previously known that Tom70 promotes the import of newly synthesized mitochondrial proteins. However, Zhou noted, the amount of protein produced must be fine-tuned to meet the needs and import capabilities of mitochondria, but not exceed production, so that excess accumulates in the cell, damaging the cells and can kill them.

In the current study, his team used yeast as a model to test whether Tom70 regulates mitochondrial biogenesis by coordinating a complex balance between the production of proteins destined for mitochondria and the rate at which these proteins can be delivered to mitochondria. They found that to be the case. A similar regulatory function of Tom70 is maintained in fruit flies.

The two processes of communication about needs and uptake in mitochondria have not previously been linked. “Our research finding that the Tom70 molecule coordinates both aspects brings together two separate areas of research,” Zhou said.

Interestingly, they found that Tom70 decreased during aging, which is associated with decreased mitochondrial biogenesis. A similar decrease in Tom70 was previously observed in older fruit flies and rats. The team further found that increasing Tom70 levels in yeast delays mitochondrial dysfunction and increases life expectancy. This discovery is due to the fact that it has been known for more than a decade that increasing Tom70 can protect human cells from certain chronic diseases such as cardiovascular disease, but the mechanistic details of why this happened were not known. “We’ve discovered a new feature for this protein, and we’re proposing a mechanism for how the Tom70 can do good things for the cell,” Zhou said.

Zhou said he could present a number of ways in which this understanding could point to new directions in the study of aging. For example, the Tom70 pathway is associated with an increase in life expectancy observed with calorie restriction. “Also, if our hypothesis turns out to be true, it will naturally lead to foods such as supplements or medications. It will just take time,” he said.

For himself, Zhou said he plans to delve deeper into yeast genetics to reveal the specifics of the mechanism, such as how the Tom70 communicates with the nucleus. “It’s the beauty of basic research, it really gives you the opportunity to explore something that didn’t exist before,” he said. “We’re excited about the translation, but we’re even more excited about something completely new that no one knew about before.”

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