A major clue to preventing mitochondrial genomic instability

April 17, 2019

Enhanced activity of the homologous recombination enzyme Mhr1 is vital

RIKEN CSRS researchers have discovered a new mechanism that prevents deletion in the mitochondrial genome (mtDNA) of budding yeast.

Mitochondria produce cellular energy through respiration, with mitochondrial DNA (mtDNA) encoding a group of proteins essential to respiratory function. When mtDNA deletion mutations occur, they create small mtDNA molecules lacking genes essential for cellular respiratory function. In humans, mtDNA deletion mutations increase with age and accumulate in cells. This phenomenon is known to be closely associated with the onset of Parkinson’s disease, cancer, and mitochondrial diseases.

RIKEN CSRS researchers found that enhanced activity of the mitochondrial homologous recombination enzyme Mhr1 in budding yeast (a model organism) prevents the loss of cellular respiratory function from such deletion mutations.

These research results open a new way toward prolonging the healthy life expectancy of humans and preventing mitochondrial diseases, which are an intractable type of genetic disease.

Original article

Scientific Reports doi:10.1038/s41598-019-41699-9

F. Ling, E. Bradshaw, M. Yoshida,

"Prevention of mitochondrial genomic instability in yeast by the mitochondrial recombinase Mhr1".

Contact

Feng Ling

Senior Research Scientist

Chemical Genomics Research Group