SOD2, the principal scavenger of mitochondrial superoxide, is dispensable for embryogenesis and imaginal tissue development but essential for adult survival

Mukherjee, Subhas; Forde, Renée; Belton, Amy; Duttaroy, Atanu

doi:10.4161/fly.5.1.14007

Cited by 19 publications

(13 citation statements)

References 48 publications

(39 reference statements)

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“…MnSOD is vital for viability in adult Drosophila , but knockout of MnSOD had no effect on embryogenesis, later development, or ifferentiation (Mukherjee et al, 2011), consistent with mouse models demonstrating that homozygous MnSOD knockout mice are normal size at birth and have no gross deformities (Li et al, 1995). Increased death rate seen in MnSOD homozygous knockout mouse neonates compared to wild-type and heterozygous MnSOD knockout littermates may be due to the inability of these mice to compensate for the high atmospheric levels of molecular oxygen compared to uterine O 2 levels.…”

Section: Mitochondria and Ros Productionsupporting

confidence: 60%

Curbing cancer's sweet tooth: Is there a role for MnSOD in regulation of the Warburg effect?

2013

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Section: Mitochondria and Ros Productionsupporting

confidence: 60%

Curbing cancer's sweet tooth: Is there a role for MnSOD in regulation of the Warburg effect?

2013

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“…Drosophila mutant for SOD2 gene, Sod2 n283 , suffers from mitochondrial dysfunction in the absence of SOD2 and generates high levels of ROS [10, 23]. A gene array analysis performed with Sod2 n283 flies and a search for oxidative stress response genes in this prooxidative environment showed that Cysu mRNA is upregulated approximately 9.37-fold higher in Sod2 n283 than in the control (Fig.…”

Section: Resultsmentioning

confidence: 99%

The essential requirement of an animal heme peroxidase protein during the wing maturation process in Drosophila

et al. 2017

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BackgroundThus far, a handful of genes have been shown to be related to the wing maturation process in insects. A novel heme peroxidase enzyme known as curly suppressor (Cysu)(formerly CG5873), have been characterized in this report because it is involved in wing morphogenesis. Using bioinformatics tools we found that Cysu is remarkably conserved in the genus Drosophila (>95%) as well as in invertebrates (>70%), although its vertebrate orthologs show poor homology. Time-lapse imaging and histochemical analyses have confirmed that the defective wing phenotype of Cysu is not a result of any underlying cellular alterations; instead, its wings fail to expand in mature adults.ResultsThe precise requirement of Cysu in wings was established by identifying a bona fide mutant of Cysu from the Bloomington Drosophila Stock Centre collection. Its requirement in the wing has also been shown by RNA knockdown of the gene. Subsequent transgenic rescue of the mutant wing phenotype with the wild-type gene confirmed the phenotype resulting from Cysu mutant. With appropriate GAL4 driver like engrailed-GAL4, the Cysu phenotype was compartmentalized, which raises a strong possibility that Cysu is not localized in the extracellular matrix (ECM); hence, Cysu is not engaged in bonding the dorsal and ventral cuticular layers. Finally, shortened lifespan of the Cysu mutant suggests it is functionally essential for other biological processes as well.Conclusion Cysu, a peroxinectin-like gene, is required during the wing maturation process in Drosophila because as a heme peroxidase, Cysu is capable of utilizing H2O2, which plays an essential role in post-eclosion wing morphogenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12861-016-0143-8) contains supplementary material, which is available to authorized users.

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“…An important approach to test the FRTA is the manipulation of SOD2. Complete deletion of SOD2 reduced the life span of Drosophila and increased neonatal mortality in mice (18,19). However, deletion of SOD2 has also been reported to increase autophagy in mouse embryonic fibroblasts (20), which is in contrast to the finding that aging is associated with a reduction in autophagy and an increase in mammalian target of rapamycin (mTOR) (21).…”

Section: Are Reactive Oxygen Species Major Contributors To Organ Dysfmentioning

confidence: 99%

Mitochondrial Hormesis and Diabetic Complications

2015

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The concept that excess superoxide production from mitochondria is the driving, initial cellular response underlying diabetes complications has been held for the past decade. However, results of antioxidant-based trials have been largely negative. In the present review, the data supporting mitochondrial superoxide as a driving force for diabetic kidney, nerve, heart, and retinal complications are reexamined, and a new concept for diabetes complications—mitochondrial hormesis—is presented. In this view, production of mitochondrial superoxide can be an indicator of healthy mitochondria and physiologic oxidative phosphorylation. Recent data suggest that in response to excess glucose exposure or nutrient stress, there is a reduction of mitochondrial superoxide, oxidative phosphorylation, and mitochondrial ATP generation in several target tissues of diabetes complications. Persistent reduction of mitochondrial oxidative phosphorylation complex activity is associated with the release of oxidants from nonmitochondrial sources and release of proinflammatory and profibrotic cytokines, and a manifestation of organ dysfunction. Restoration of mitochondrial function and superoxide production via activation of AMPK has now been associated with improvement in markers of renal, cardiovascular, and neuronal dysfunction with diabetes. With this Perspective, approaches that stimulate AMPK and PGC1α via exercise, caloric restriction, and medications result in stimulation of mitochondrial oxidative phosphorylation activity, restore physiologic mitochondrial superoxide production, and promote organ healing.

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SOD2, the principal scavenger of mitochondrial superoxide, is dispensable for embryogenesis and imaginal tissue development but essential for adult survival

Cited by 19 publications

References 48 publications

Curbing cancer's sweet tooth: Is there a role for MnSOD in regulation of the Warburg effect?

Curbing cancer's sweet tooth: Is there a role for MnSOD in regulation of the Warburg effect?

The essential requirement of an animal heme peroxidase protein during the wing maturation process in Drosophila

Mitochondrial Hormesis and Diabetic Complications

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