sod-3

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Genetic mutants with sod-3 alterations

Temperature °C
20
Lifespan (days)
21.5
Lifespan change (compared to wild type)
-5.29%
Lifespan comparisons
Single mutant sod-3(sj134) has a lifespan of 21.5 days, while wild type has a lifespan of 22.7 days.
Citation
View abstract
Honda Y et al., 2008, Modulation of longevity and diapause by redox regulation mechanisms under the insulin-like signaling control in Caenorhabditis elegans. Exp Gerontol. 43(6):520-9 18406553 Click here to select all mutants from this PubMed ID in the graph
Abstract
In Caenorhabditis elegans, the downregulation of insulin-like signaling induces lifespan extension (Age) and the constitutive formation of dauer larvae (Daf-c). This also causes resistance to oxidative stress (Oxr) and other stress stimuli and enhances the expression of many stress-defense-related enzymes such as Mn superoxide dismutase (SOD) that functions to remove reactive oxygen species in mitochondria. To elucidate the roles of the two isoforms of MnSOD, SOD-2 and SOD-3, in the Age, Daf-c and Oxr phenotypes, we investigated the effects of a gene knockout of MnSODs on them in the daf-2 (insulin-like receptor) mutants that lower insulin-like signaling. In our current report, we demonstrate that double deletions of two MnSOD genes induce oxidative-stress sensitivity and thus ablate Oxr, but do not abolish Age in the daf-2 mutant background. This indicates that Oxr is not the underlying cause of Age and that oxidative stress is not necessarily a limiting factor for longevity. Interestingly, deletions in the sod-2 and sod-3 genes suppressed and stimulated, respectively, both Age and Daf-c. In addition, the sod-2/sod-3 double deletions stimulated these phenotypes in a similar manner to the sod-3 deletion, suggesting that the regulatory pathway consists of two MnSOD isoforms. Furthermore, hyperoxic and hypoxic conditions affected Daf-c in the MnSOD-deleted daf-2 mutants. We thus conclude that the MnSOD systems in C. elegans fine-tune the insulin-like-signaling based regulation of both longevity and dauer formation by acting not as antioxidants but as physiological-redox-signaling modulators.

Temperature °C
20
Lifespan (days)
17.1
Lifespan change (compared to wild type)
-3.39%
Lifespan comparisons
Single mutant sod-3(tm760) has a lifespan of 17.1 days, while wild type has a lifespan of 17.7 days.
Citation
View abstract
Van Raamsdonk JM, Hekimi S, 2009, Deletion of the mitochondrial superoxide dismutase sod-2 extends lifespan in Caenorhabditis elegans. PLoS Genet. 5(2):e1000361 19197346 Click here to select all mutants from this PubMed ID in the graph
Abstract
The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, flies, and mice results in decreased lifespan. In this experiment, we examine the effect of eliminating each of the five individual sod genes present in Caenorhabditis elegans. In contrast to what is observed in other model organisms, none of the sod deletion mutants shows decreased lifespan compared to wild-type worms, despite a clear increase in sensitivity to paraquat- and juglone-induced oxidative stress. In fact, even mutants lacking combinations of two or three sod genes survive at least as long as wild-type worms. Examination of gene expression in these mutants reveals mild compensatory up-regulation of other sod genes. Interestingly, we find that sod-2 mutants are long-lived despite a significant increase in oxidatively damaged proteins. Testing the effect of sod-2 deletion on known pathways of lifespan extension reveals a clear interaction with genes that affect mitochondrial function: sod-2 deletion markedly increases lifespan in clk-1 worms while clearly decreasing the lifespan of isp-1 worms. Combined with the mitochondrial localization of SOD-2 and the fact that sod-2 mutant worms exhibit phenotypes that are characteristic of long-lived mitochondrial mutants-including slow development, low brood size, and slow defecation-this suggests that deletion of sod-2 extends lifespan through a similar mechanism. This conclusion is supported by our demonstration of decreased oxygen consumption in sod-2 mutant worms. Overall, we show that increased oxidative stress caused by deletion of sod genes does not result in decreased lifespan in C. elegans and that deletion of sod-2 extends worm lifespan by altering mitochondrial function.

Search genes: sod-3

Entrez ID
Symbol
GenAge
Wormbase ID

181748
sod-3
View on GenAge (sod-3)
WBGene00004932

Superoxide dismutase [Mn] 2, mitochondrial

Locus: CELE_C08A9.1

Wormbase description: sod-3 encodes a iron/manganese superoxide dismutase, predicted to be mitochondrial, that might defend against oxidative stress and promote normal lifespan; sod-3 mRNA levels are diminished by mutation of daf-16 and chromatin immunoprecipitation (ChIP) studies demonstrate that DAF-16 can directly bind the sod-3 promoter; heterologously expressed SOD-3 in E. coli protects against methyl viologen-induced oxidative stress.

Orthologs of sod-3 in SynergyAge

Show in SynergyAge
Species	Gene
Drosophila melanogaster	Sod2

Not in SynergyAge
Species	Gene
Mus musculus	Sod2