The new molecular sciences continue to delve deeper into the mysteries of the cellular actions and interactions to unlock the keys to PARKINSON’S DISEASE. A team of genetic researchers at the University of California at Los Angeles headed by Dr. Ming Guo has found one more clue, a gene that mediates the interactions of two mutated genes and helps cells maintain their health to prevent neurodegeneration.
The genes PINK1and Parkin play important roles in protecting the energy producing mitochondria of cells. When these genes are mutated, they do not operate correctly and allow for accumulations of unhealthy cells with damaged mitochondria that leads to the early on-set of PARKINSON’S DISEASE. Working in fruit flies and mouse models of disease, Guo and her team found that a gene called MUL-1 mediated the interaction of PINK-1 and Parkin and contributed to the health of the mitochondria. When MUL-1 was removed from the interaction with PINK-1 and Parkin in the neurons in the mouse model, they found it caused deterioration of the mitochondria, but when an extra amount of MUL-1 was added, the mitochondrial damage was repaired.
The discovery of this new genetic interaction is exciting, showing a new mechanism for improving the function of mitochondria and maintaining the health of the cell, but also because it may lead to the development of a drug that could enhance its presence and prevent neurodegeneration. Such a new drug would be of immense benefit to people with PARKINSON’S DISEASE.
Further studies will test these findings in more complex biological organisms and will help to find more cellular interactions related to MUL-1. Testing for drugs that will enhance MUL-1 and become a basis for treatment is another a priority. The team will also be looking for mutations of the MUL-1 gene and to understand its heritability to see if it exists in all PARKINSON’S patients or if it is found only in the inherited forms of PARKINSON’S.
J. Yun, R. Puri, H. Yang, M. A. Lizzio, C. Wu, Z.-H. Sheng, M. Guo. MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkin. eLife, 2014; 3 (0): e01958 DOI:10.7554/eLife.01958
Review by Marcia McCall
Picture Credits
No comments:
Post a Comment