Is There a Link Between Cytoskeletal Proteins, Mitochondria Length and Neurodegenerative Diseases?

A recent discovery out of Dr. Henry Higgs’ laboratory at Dartmouth’s Geisel School of Medicine, and reported in the January 25th issue of Science, sheds light on the dynamics of mitochondrial fission and fusion. INF2 (Inverted Formin 2) normally regulates actin polymerization, so the researchers were surprised to find that INF2 could also influence mitochondrial length. Silencing INF2 using small interfering RNAs led to an increase in the average length of  mitochondria. Furthermore, when the researchers overexpressed a mutant version of INF2, the mitochondria decreased in size. Mutations in INF2 have been associated with Charcot-Marie-Tooth Disease (CMTD), and this research provides additional insights into the role that cytoskeletal and mitochondrial dynamics may have in CMTD, as well as in other neurodegenerative diseases. As Dr. Higgs said, "before this discovery, no one thought the cytoskeleton played a role in mitochondrial division." Read more about these striking findings here.

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