2017
DOI: 10.1016/j.freeradbiomed.2017.04.004
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Abstract: Mutations affecting components of the mitochondrial electron transport chain have been shown to increase lifespan in multiple species including the worm Caenorhabditis elegans. While it was originally proposed that decreased generation of reactive oxygen species (ROS) resulting from lower rates of electron transport could account for the observed increase in lifespan, recent evidence indicates that ROS levels are increased in at least some of these long-lived mitochondrial mutants. Here, we show that the long-… Show more

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Cited by 58 publications
(63 citation statements)
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References 52 publications
(74 reference statements)
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“…The mitochondrial dynamics mutants also showed slow development, slow movement (thrashing rate), and a slow rate of defecation. These phenotypes have also been observed in other mitochondrial mutants such as clk‐1, isp‐1, and nuo‐6, 20,21,34‐36 and may be at least partially explained by the observed reduction in ATP levels.…”
Section: Discussionsupporting
confidence: 63%
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“…The mitochondrial dynamics mutants also showed slow development, slow movement (thrashing rate), and a slow rate of defecation. These phenotypes have also been observed in other mitochondrial mutants such as clk‐1, isp‐1, and nuo‐6, 20,21,34‐36 and may be at least partially explained by the observed reduction in ATP levels.…”
Section: Discussionsupporting
confidence: 63%
“…Having shown that mitochondrial morphology and function are disrupted in mitochondrial fission and fusion mutants, we investigated whether these deficits lead to an alteration of physiologic rates. Previous studies have demonstrated that mutations affecting the mitochondria often cause a slowing of physiologic rates 20,21,34‐36 . While wild‐type worms exhibit essentially no embryonic lethality, we found that almost 50% of drp‐1 eggs and over 10% of eat‐3 and fzo‐1 eggs fail to hatch indicating an increased rate of embryonic lethality (Figure 3A).…”
Section: Resultsmentioning
confidence: 47%
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“…Moreover, different molecular players have been identified in the past two decades that mediate Mit mutants' longevity: a handful of transcription factors [7,[17][18][19][20][21][22], autophagy-and apoptosis-regulatory genes [7,14,18,23,24], some kinases [25][26][27], as well as some mitochondrial metabolites [28] and chromatin remodeling genes [29,30]. Nonetheless, whether the same molecular mechanisms underlie the different Mit-mutant's phenotypic features is largely unknown [14,31,32]. The C. elegans p53 ortholog, cep-1, specifies many of the Mitmutant phenotypes, including animal's reduced fertility and germline size [14,17,18,33], and mediates germ-cell apoptosis in response to genotoxic stress [34,35].…”
Section: Introductionmentioning
confidence: 99%
“…Alternatively, decreased neuropeptide secretion could result from activation of stress response pathways. Several stress response pathways are induced in mitochondrial mutants, including those mediated by the hypoxia inducible factor (HIF-1), SKN-1/Nrf2, the mitochondrial unfolded protein response, and the AMP activated protein kinase (SENA AND CHANDEL 2012;HWANG et al 2014;BLACKWELL et al 2015;CHANG et al 2017;DUES et al 2017; SHPILKA AND HAYNES 2018).…”
Section: Hypoxia Inhibits Neuropeptide Secretionmentioning
confidence: 99%