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Genetically Modified Fruit Fly Study Points to ER Protein Role in Motor Disorder, Heart Rate

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."