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Keywords {🔍}

mitochondrial, fission, mitochondria, cell, bax, neurons, snoc, death, article, neuronal, figure, cas, google, scholar, foci, formation, mfn, egfpbax, exposure, cultures, morphology, cortical, stress, bclxl, dsredmito, nitric, nature, nitrosative, drpka, fusion, membrane, number, drp, neuron, oxide, volume, data, image, atp, activation, size, snocinduced, length, min, control, biol, results, effects, images, cells,

Topics {✒️}

nature portfolio alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors permissions reprints privacy policy secondary nature nature advertising blocked n-methyl-d-aspartate social media amp-activated protein kinase 1 mg/ml poly-l-lysine n-methyl-d-aspartate antiapoptotic bcl-xl failed dsred2-mito/egfp-bax colocalization dynamin-related protein drp1 pentylenetetrazole-induced clonic seizures cell death-related events charcot-maric-tooth-type2a intracellular power-transmitting cables imaging research greater capillary-fiber interface hepes-buffered salt solution life scientific fisher scientific wolfram research medical research nitric oxide-induced apoptosis nmda receptor-channel complex full size image caspase-independent cell death mitochondrial fission/fusion machinery dynamin-related protein 1 bcl-xl blocks cytochrome ice-cold distilled water egfp-bax pattern changed snoc-induced mitochondrial fission bcl-2 related proteins voltage-gated ca2+ channels adenine nucleotide translocase dynamin-related gtpases nitric oxide production author correspondence plasmids encoding dsred2-mito antiapoptotic bcl-xl fccp-induced mitochondrial shortening dsred2-mito selectively traces high-resolution fluorescence imaging plasmids encoding egfp-bax distinct events induced neurons expressing dsred2-mito

Questions {❓}

• A specific method for activating AMP-activated protein kinase in intact cells?
• How does NO evoke mitochondrial fission?
• How does mitochondrial fission lead to neurodegeneration?
• What is the role of mitochondrial fission in the execution program of cell death?

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      description:Mitochondrial dysfunction is an underpinning event in many neurodegenerative disorders. Less clear, however, is how mitochondria become injured during neuronal demise. Nitric oxide (NO) evokes rapid mitochondrial fission in cortical neurons. Interestingly, proapoptotic Bax relocates from the cytoplasm into large foci on mitochondrial scission sites in response to nitrosative stress. Antiapoptotic Bcl-xL does not prevent mitochondrial fission despite its ability to block Bax puncta formation on mitochondria and to mitigate neuronal cell death. Mitofusin 1 (Mfn1) or dominant-negative dynamin-related protein 1K38A (Drp1k38A) inhibits mitochondrial fission and Bax accumulation on mitochondria induced by exposure to an NO donor. Although NO is known to cause a bioenergetic crisis, lowering ATP by glycolytic or mitochondrial inhibitors neither induces mitochondrial fission nor Bax foci formation on mitochondria. Taken together, these data indicate that the mitochondrial fission machinery acts upstream of the Bcl-2 family of proteins in neurons challenged with nitrosative stress.
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