Researchers at the University of Bonn and other centers consider the consequences of knocking out a "cysteine-rich with EGF-like domain" (Creld) endoplasmic reticulum (ER) gene previously implicated in Parkinson's disease for a paper in Science Advances. Using genetically modified Drosophila fruit fly models, the team detected slower-than-usual heart rates and severe motor disorder symptoms in flies missing Creld, consistent with ties between the ER protein and the function of energy producing mitochondrial organelles in the cell — findings validated in Xenopus tropicalis claw frog embryos and human cell experiments. Through a series of follow-up analyses, the authors saw signs that such symptoms may stem from altered ER-mitochondria interactions and related mitochondrial respiratory complex activity shifts. "We found that loss of Creld leads to mitochondrial hyperfusion and reduced [reactive oxygen signaling] signaling in Drosophila melanogaster, Xenopus tropicalis, and human cells," they report, noting that resulting hydrogen peroxide level dips "are linked to disturbed neuronal activity and lead to impaired locomotion."
Genetically Modified Fruit Fly Study Points to ER Protein Role in Motor Disorder, Heart Rate
Jul 25, 2022