Mayer Foundation, the Renee and Meyer Luskin Family Fund, the B. The study was funded by the National Institutes of Health, the Wellcome Trust, the Glenn Foundation for Medical Research, the Louis B. Craig Blackstone of Harvard Medical School and Robert Harvey of the University of Sunshine Coast in Australia. Other authors are Jina Yun, a former UCLA postdoctoral researcher Caroline Sibilla, a former graduate student at the National Institutes of Health Raymond Liu, Bruce Hay and David Chan of Caltech Dr. The study’s first author is Huan Yang, a UCLA postdoctoral researcher. Harvey and Ming Guo, 24 March 2022, Nature Communications. Reference: “Clueless/CLUH regulates mitochondrial fission by promoting recruitment of Drp1 to 6 mitochondria” by Huan Yang, Caroline Sibilla, Raymond Liu, Jina Yun, Bruce A. “In the future, we hope to identify a mechanism with such precision that it only affects Parkinson’s disease, so patients can derive maximum benefit,” she said. Guo’s research group is continuing to investigate how CLUH controls mitochondrial fission and its impact in cellular and organism health. More available Drp1 receptors means that more Drp1 can be recruited in order to trigger fission. In addition, the researchers discovered that CLUH in human cells helps translate the genetic instructions found in messenger RNA into the protein for Drp1 receptors on the surface of mitochondria. The team further showed that both clueless in flies and CLUH in human cells recruit free-floating Drp1 from within a cell to attach to receptors on the surface of mitochondria. That striking recovery indicated that clueless’s ability to control mitochondrial fission works through Drp1. Guo said the longer mitochondria likely result from too little fission, and the fragmented ones from too much fission.įruit flies that had been genetically engineered to lack clueless - a manipulation that dramatically shortens their lifespans - lived up to nearly four times as long when the researchers administered more Drp1 protein. Guo and her colleagues found that the loss of clueless (in the fruit flies) or CLUH (in the human cells) resulted in mitochondria that appeared to be longer, while large amounts of clueless or CLUH proteins resulted in fragmented mitochondria. Cell-free environments enable scientists to observe interactions between proteins in a simple context. The researchers investigated complex biochemical chain reactions in fruit flies, in human cell cultures and among proteins in a cell-free environment. “These findings should provide significant insight to the scientific community, not only into understanding fundamental principles of biology but also for improving human health,” said Guo, who is also a member of the California NanoSystems Institute at UCLA. Guo’s research focuses on neurodegenerative conditions, but disruptions in the fission of mitochondria are behind a host of other ailments, including cancer, diabetes and heart disease, as well as some developmental defects that lead to infants’ death. Ming Guo, the corresponding author of the study and a professor of neurology and of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA. “When we modified clueless in flies, symptoms analogous to Parkinson’s disease improved substantially.” “With a critically important pathway such as Drp1, there might be multiple proteins we could use to intervene and ultimately control Parkinson’s disease,” said Dr. In experiments with fruit flies that were genetically engineered with an analog for Parkinson’s disease, the team showed that damage from the disease could be reversed by increasing the amount of a protein that scientists call “clueless,” which is the fruit fly equivalent of CLUH. The study, published today (March 24, 2022) in Nature Communications, found that a protein in humans called CLUH (pronounced “clue-H”) acts to attract Drp1 to mitochondria and trigger fission. Ming Guo, the corresponding author of the study and a professor of neurology and of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA.
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