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Abstract:This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
“… 37 , 60 Wild type animals maintained a constant basal OCR from the young adult stage to day 6 of adulthood, although a tendency to reduce basal respiration during aging was apparent, as previously reported ( Figure 5 A, compare YA to D6). 61 , 62 By contrast, as sin-3 mutants aged, basal OCR dramatically increased, so that at day six of adulthood it was more than 2-fold higher in sin-3 mutants compared to wild type ( Figure 5 A, D6). Figure 5 Oxygen consumption rate (OCR) and abundance of mitochondrial respiratory chain subunits in sin-3(tm1276) mutants (A) Basal OCR of wild type and sin-3 mutants at the young adult (YA) stage and at day 6 of adulthood (D6).…”
“… 37 , 60 Wild type animals maintained a constant basal OCR from the young adult stage to day 6 of adulthood, although a tendency to reduce basal respiration during aging was apparent, as previously reported ( Figure 5 A, compare YA to D6). 61 , 62 By contrast, as sin-3 mutants aged, basal OCR dramatically increased, so that at day six of adulthood it was more than 2-fold higher in sin-3 mutants compared to wild type ( Figure 5 A, D6). Figure 5 Oxygen consumption rate (OCR) and abundance of mitochondrial respiratory chain subunits in sin-3(tm1276) mutants (A) Basal OCR of wild type and sin-3 mutants at the young adult (YA) stage and at day 6 of adulthood (D6).…”
“…Ultimately, these dysfunctions contribute to cellular demise and cell death 23 . Moreover, our recent findings indicate that Ca 2+ overload promotes mitophagy and results in mitochondrial volume loss in C. elegans BWMC 15 . Both genetic ( mcu-1 mutation) and pharmacological (Ru360 administration) suppression of MCU can ameliorate muscle weakness induced by C. elegans aging and dys-1 (eg33) mutation of DMD model 15 .…”
mentioning
confidence: 84%
“…1d, f ). Furthermore, when compared to the mitochondrial calcium uniporter (MCU) inhibitor Ru360 15 , MA-5 did not inhibit mitochondrial Ca 2+ oscillations synchronized with cytoplasmic Ca 2+ oscillations during the muscular contraction and relaxation cycle in C. elegans BWMC (Supplementary Fig. 1 ).…”
mentioning
confidence: 98%
“…1d, e ). We recently found that mitochondrial Ca 2+ ([Ca 2+ ] mito ) levels in BWMC increase with age by using the aceIs1 transgene of mitochondrial Ca 2+ sensor mtLAR-GECO (strain ATU3301) 15 . Remarkably, the administration of MA-5 was able to suppress the age-related elevation in [Ca 2+ ] mito levels (Fig.…”
Mitochonic acid-5 ameliorates the pathophysiology of human mitochondrial-disease fibroblasts and Caenorhabditis elegans Duchenne muscular dystrophy and Parkinson’s disease models. Here, we found that 10 μM MA-5 attenuates the age-related decline in motor performance, loss of muscle mitochondria, and degeneration of dopaminergic neurons associated with mitochondrial Ca2+ overload in C. elegans. These findings suggest that MA-5 may act as an anti-aging agent against a wide range of neuromuscular dysfunctions in metazoans.
“…In C. elegans , the complex consists of the channel protein MCU-1, along with two regulatory subunit proteins MICU-1 and EMRE-1. With the molecular identity revealed a little more than a decade ago 14,15 , studies are beginning to uncover its various roles in different tissues during normal and pathological conditions 16,17 . Similarly, their function in neurons is only beginning to be understood.…”
Despite growing understanding of the various roles mitochondria play in neurons, how they contribute to higher brain functions such as learning and memory remains underexplored. Here, using C. elegans, we found that expression level and activity of the mitochondrial calcium uniporter (MCU) pore forming unit MCU-1 impacts learning and memory for odors sensed by a specific sensory neuron, AWCON. Genetic and pharmacological manipulation showed that MCU-1 was required in the sensory neuron during conditioning. For aversive odor learning, MCU-1 mediates learning to 60-min conditioning by facilitating the selective release of NLP-1 neuropeptide through mitochondrial ROS production. MCU activation and neuropeptide release likely coincide with the AWC calcium peak following odor removal. We propose that mitochondria contribute to learning and memory by acting as a duration sensor to control select neuropeptide release in response to prolonged stimuli.
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