Scientists believe that mitochondria used to be an independent single-celled organism, and it was not swallowed up by larger cells until more than 654.38 billion years ago. In this way, they avoided the bad luck of being digested, established a mutually beneficial relationship with their hosts, and finally led to the emergence of more complex life such as animals and plants.
After a long evolution, the mitochondrial genome has shrunk. Nowadays, the nucleus contains the vast majority of cellular genetic material, and even the genes that provide services for mitochondria. Over time, most mitochondrial genes jumped into the nucleus. However, if these genes are mobile, why do mitochondria keep them, especially the mutation of these genes will lead to serious rare diseases and gradually destroy the important organs such as brain, liver and heart of patients?
Ian Johnston, a biologist at the University of Birmingham in the United Kingdom, and Ben Williams, a biologist at the whitehead Institute of Biomedicine in Cambridge, Massachusetts, jointly compared various hypotheses through mathematical modeling for the first time. They analyzed more than 2000 different mitochondrial genomes from animals, plants, fungi and protozoa (such as amoeba), and traced their evolutionary paths, thus creating a program to calculate the probability of different genes and genomes being lost at a specific point in time.
Keith Adams, a biologist at the University of British Columbia in Vancouver, Canada, was not involved in the study, but he said: "The conventional practice of this kind of research does not include modeling methods, which is a reflection of many innovations in this project."
Mitochondria transfer electrons along the cell membrane through a series of chemical reactions to generate energy. The key to this process is that a series of protein complexes and macroglobulins are embedded in the inner membrane of mitochondria. The team found that if the protein produced by the gene is at the core of the protein complex, the gene is more likely to be preserved. At the same time, genes responsible for generating more energy for the periphery are more likely to be transported to the nucleus.
Johnston believes that keeping these genes in mitochondria is a unique way for cells to control mitochondria, because the key protein is produced in mitochondria. This local control means that cells can regulate the instantaneous energy production in a single mitochondria more quickly and effectively without making large-scale changes to hundreds or even thousands of mitochondria.
John Allen, a biologist at University College London who is not a member of the project team, said that this is the same as people's reaction to fire. If a room in a huge building catches fire, people will choose to pick up the fire extinguisher and put it out directly instead of calling the building manager to send out a fire extinguishing request.
He also said: "I think this is a very basic feedback mechanism." His research found that as long as some mitochondrial proteins are produced where necessary, it can help cells to better regulate energy production. Other structures in our cells can also benefit from this local control. But mitochondria, as once independent cells, are the only cells with independent command centers.
The research model of Johnston and Williams also reflects some other aspects that may be of great significance. For example, genes encoding the hydrophobicity or waterproofness of mitochondrial protein are more likely to be produced in mitochondria. This is because if these protein are produced elsewhere in the cell, they may sometimes be blocked in transportation.
The chemical structure of the gene itself will also affect whether it can be preserved. Those genes that can resist the harsh environment inside mitochondria and are not easily damaged are more likely to remain.
Johnston believes that the computer program developed by him and Williams can be used in many aspects other than mitochondrial genome screening. The algorithm can analyze any problem that the pathogenic gene or disease symptom gains or loses some characteristics at a certain time node. He hoped that the model would be helpful to the prediction of the follow-up study.
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