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General Information
Symbol
Dmel\Sod1n1
Species
D. melanogaster
Name
FlyBase ID
FBal0015933
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
cSODn108, Sod1n108, Sodn1, SODn108
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G11112767A

Amino acid change:

G50S | Sod1-PA

Reported amino acid change:
Comment:

mutant coordinates reported in FBrf008426 based on nucleotide coordinates in FBrf0047097.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: G49S.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Sodn1 mutant glia exhibit lipid droplet accumulation.

Homozygous Sodn1 mutants are viable.

Compared to controls, Sodn1 mutant larvae show significantly higher oxidative DNA damage after the addition of DDVP (0.15-15.0ng/ml).

The supplementation of algal cells (from Haematococcus pluvialis) at high concentrations (10 and 20mg/mL) significantly extends the life span of Sodn1 mutant flies (while this concentration appears to be toxic to control flies). Low concentrations of algal cells do not have a significant effect on the life span of Sodn1 mutant flies.

The age-dependent decline in locomotor function in Sodn1 mutant flies is effectively rescued by the intake of Haematococcus pluvialis cells.

The lifespan of homozygous Sodn1 mutants is shorter than than of controls.

Chronic hypoxia (5% O[[2]]) partially restores the abbreviated life span of mutant flies.

Homozygous flies show a reduction in adult lifespan compared to controls and are extremely hypersensitive to paraquat.

Homozygotes have a significantly shorter mean and maximum life span than normal; mean life span of the mutants is 12 days (compared to 40 days for controls) and maximum lifespan of the mutants is 24 days (compared to 70 days for controls).

Homozygous male escapers are sterile and female escapers have reduced fertility. Escapers have reduced longevity and are sensitive to paraquat, buthionine sulfoximine, ionising radiation and hyperoxia compared to control flies.

In Sodn1 eggs of L.boulardi are melanotically encapsulated but, in contrast to the wild-type, survive.

Homozygous adult eye has extensive necrotic lesions throughout the retina. Histological defects also extend into the adjacent lamina of the brain. This neuropathology is consistent with behavioural defects, including motor activity.

Homozygous larvae are poorly viable at 31oC.

Homozygotes that are also homozygous for ry301 or ry506 die during late metamorphosis and during the process of eclosion.

Homozygotes life span is 80% less than wild type.

Originally recovered as a lethal mutation; homozygotes die in the process of eclosion; rare eclosing adults are completely sterile, are devoid of SOD activity and die within 2-3 days; however, some derived sublines show higher adult survival. Surviving homozygous males are sterile and homozygous females produce few if any offspring. Reduced life span and fertility attributed to reduced capacity of embryos, larvae, and pupae to protect developing preimaginal cells from O2--initiated cytotoxic damage. Homozygotes hypersensitive to the O2--radical-generating compound, paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride) and copper ions.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

Sod1n1/Sod1n64 has short lived phenotype, enhanceable by Wwox1/Wwox1

Enhancer of
Statement
Reference

Sod1n1/Sod[+] is an enhancer of paralytic phenotype of Hsap\GFAPUAS.cWa, Scer\GAL4repo

Sod1n1/Sod[+] is an enhancer of lethal | recessive phenotype of Trxr-1G0481

Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhancer of
Statement
Reference

Sod1n1/Sod[+] is an enhancer of lamina phenotype of Hsap\GFAPUAS.cWa, Scer\GAL4repo

Sod1n1/Sod[+] is an enhancer of adult brain phenotype of Hsap\GFAPUAS.cWa, Scer\GAL4repo

NOT Enhancer of
Statement
Reference

Sod1n1/Sod[+] is a non-enhancer of eye phenotype of cathD1

Additional Comments
Genetic Interactions
Statement
Reference

Sodn1/Sodn64 Wwox1/Wwox1 double mutant adult escapers show further reduction of the shortened lifespan seen in Sodn1/Sodn64 single mutant adults.

qvr1/+ ; Sodn1/Sodn1 and qvr1/qvr1 ; Sodn1/Sodn1 animals die as late pupae. Sh5, Hk1 and eag1 double mutants with Sodn1 are viable.

Xenogenetic Interactions
Statement
Reference

A Sodn1 heterozygous background significantly enhances Hsap\GFAPScer\UAS.cWa toxicity and increases the frequency of mechanically-stimulated seizures in these flies. Protection from cellular toxicity does not alter the number of inclusion bodies. An increase in cellular toxicity does not alter the number of inclusion bodies but does increase autophagy induction.

A Sodn1 heterozygous background significantly enhances Hsap\GFAPR79H.Scer\UAS toxicity and increases the frequency of mechanically-stimulated seizures in these flies. Protection from cellular toxicity does not alter the number of inclusion bodies. An increase in cellular toxicity does not alter the number of inclusion bodies but does increase autophagy induction.

Sodn1 dominantly suppresses the decreased survival phenotype of flies expressing Hsap\APPArctic.Scer\UAS.T:nec under the control of Scer\GAL4elav-C155.

Expression of P{bSOD} restores male fertility and resistance to paraquat to apparently normal levels. Adult life is restored to only 30% of normal and resistance to hyperoxia is 90% of that found in control flies.

Complementation and Rescue Data
Rescued by
Comments

SodF.tSa rescues the lethality of Sodn1 homozygotes. The rescued flies are fertile and longevity is essentially wild-type. The rescued flies have a wild-type level of resistance to paraquat and an increased resistance to hyperoxia compared to control flies. Sensitivity to ionising radiation is partially rescued. Sensitivity to buthionine sulfoximine is rescued.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (19)
References (36)