Studies of cells have revealed that mitochondria are a sure signal of cellular stress. Times when invaded by viruses and mutations, this signals the release of ISGs that protect and kill the invading proteins. Without this mechanism, cells will be very vulnerable.
This DNA is the key to keep a cell healthy, cancer and other severe genetic diseases are caused by mutated DNA. Many scientists are now finding ways to enact cures at the DNA level, to correct badly replicated proteins.
One problem, though it does not always manifest the alteration of the DNA or proteins, nature has built-in a wonderful device to spot them (mitochondrion). That built defense that sounds the starting signs of cellular stress or attack is the mitochondria. Mitochondria are needed by cells and are one of the most archaic parts of the first single-celled creatures. Researchers Gerald Shadel who works as a professor in Salk's Molecular and Cell Biology Laboratory, chair in Biomedical Science made these remarks on the importance of mitochondria, as one of the cell's most vital structure.
Inside the cell, there is already DNA information packed inside it, but the mitochondria have its own store of DNA inside it. This is called mitochondrial DNA or mtDNA, which is transmitted from the mother to the children. This is like a second set of packed DNA inside the mitochondria which also produced proteins to power the functions of the cells too.
Experiments by Dr. Shadel has demonstrated that cell will respond to mutated mtDNA by sounding the alarm inside the cell. Instant response by the cell is to send mtDNA as a corrective measure to boost immune-defense mechanisms inside the cell. This bulks up the resistance, to any invader trying to corrupt cell functions.
How this cellular mechanism works, is examined by scientists to understand it more. Structures that are getting more interest are the molecular passages that are opened when faulty mtDNA enters the cell. One of these notable genes is interferon-stimulated genes or ISGs, that sprang to action one viral or mutated material that has bypassed the cell's membrane. They are the same ISGs that are active when cancerous cells are resistant to chemo, and doxyrubicin is destroying the cell's DNA.
Ironically, the doxyrubicin (anti-cancer drug) does not only destroy the cancer cells' nuclear DNA, but it will also damage the DNA and mtDNA then ISGs will start working. By tripping the ISGs, the anti-cancer drug will be resisted by the activity of the ISGs. An end result is that treatment for cancer is foiled by the cellular processes that destroy bad proteins.
When the mitochondria are looked at closely, it exhibited more stress than usual. Like a chain reaction, the cells were not receptive to the drug, limiting its efficacy too. One characteristic is more ISGs were on alert, guard the cells nuclear DNA keeping the mutated proteins working. Instead of the anti-cancer drug entering the cell and correcting the problem.
The conclusion reached by the study is that mitochondrial is replicated inside a cell many times, but has fewer DNA passages. Fewer passages in the mtDNA will cause any viral or mutation invading the cell to activate ISGs because of cellular stress. It is the release of ISGs that works both ways, one to kill the virus and to repair the damage. Without the susceptibility to damage mitochondrial DNA (mtDNA), the detecting mechanisms might not be enough, this helps to restore parts of a damaged cell.
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