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General Information
Symbol
Dmel\DreddB118
Species
D. melanogaster
Name
FlyBase ID
FBal0120966
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C635067T

Amino acid change:

R105term | Dredd-PD; R105term | Dredd-PE; R105term | Dredd-PF; R51term | Dredd-PG

Reported amino acid change:

R127term

Comment:

The predicted amino acid change was reported relative to a 516aa Dredd protein, which would be created by the use of an uptream translation start. The current Dredd genome annotation uses a downstream AUG which is supported by both species conservation and RNA-seq data. The two start sites are 22 aa apart.

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

Amino acid replacement: R127term.

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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

As measured by H[[2]]O[[2]] ingestion, DreddB118 mutants are more resistant to oxidative stress than wild-type.

In the absence of infection, DreddB118 mutants have rates of intestinal stem cell division that is at least three time as high as those of control flies.

There is no significant difference in bacterial load after infection with Vibrio cholerae between control and mutant flies.

DreddB118 mutant flies upon continuous light exposure for 6 days show visible changes in retinal morphology (increase in intraommatidial space, reduced rhabdomeres size, and loss of rhabdomeres in some photoreceptors) while no retinal morphological changes are seen in dark-raised flies as compared to WT control.

Mutant flies show greatly reduced survival compared to wild type after septic injury with Erwinia carotovora carotovora 15.

DreddB118 homozygotes exhibit wild-type apoptosis of vCrz neurons, with no viable vCrz neurons detected at 7 hours after puparium formation.

Homozygous and hemizygous flies are resistant to V. cholerae infection compared to controls.

24 hours after infection with V. cholerae, the bacterial load of homozygous mutants is comparable to or greater than controls - resistance is not the result of decreased colonization.

Homozygous mutants are slightly more susceptible to infection by V. cholerae by septic injury compared to controls.

24 hours after infection with V. cholerae, homozygous mutants show increased apoptosis in the intestine compared to controls.

Developmental apoptosis is normal in embryos that are maternally and zygotically mutant for DreddB118.

Developmental apoptosis is normal in homozygous third instar eye discs.

γ-ray induced apoptosis is not suppressed in homozygous third instar wing discs.

High mortality levels are observed when DreddB118 flies are fed on the ROS-resistant KNU53775 yeast strain but are not observed when they are fed on a standard yeast strain (W303). Wild-type flies do not show the same sensitivity to the KNU53775 strain. The number of KNU53775 microbes is ~100 times higher in the intestines of DreddB118 flies than in controls.

DreddB118 flies show increased mortality following infection with a Salmonella strain that overexpresses an antioxidant gene, but these flies show no increased mortality following infection with the same Salmonella stain but without antioxidant overexpression. There is a marked microbial persistance of oxidant-overexpressing Salmonella in the intestines of DreddB118 flies compared to controls.

Mutant flies show similar survival rates as control flies following natural infection (feeding with contaminated food) with either "Ecc-15" (P.carotovorum.carotovorum), S.cerevisiae or M.luteus.

DreddB118 flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).

Defects are seen in the movement of investment cones in mutant spermatid, which normally move tailwards in a co-ordinated fashion. In about half of cysts from mutant testes display defects in individualisation. In other cysts individually occurs apparently normal.

Mutant animals have an increased susceptibility to E.coli infection. 30 and 40% of homozygous and heterozygous mutants survive respectively.

Mutant flies are more susceptible to infection by the Gram negative bacterium Erwinia carotovora than controls.

Mutant animals are highly susceptible to Gram-negative bacterial infection, exhibiting a dramatic loss of survival rate after infection, with all animals dying within 3 days.

Mutant adults are highly susceptible to infection by E.coli (survival rate is reduced after pricking with an infected needle compared to survival rate of control flies). Mutant adults are not highly susceptible to infection by M.luteus.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Phenotype Manifest In
NOT Enhancer of
Statement
Reference

DreddB118 is a non-enhancer of neuron phenotype of DroncI24, Strica4

Suppressor of
Statement
Reference

DreddB118 is a suppressor of retina | progressive | conditional phenotype of norpA7

DreddB118 is a suppressor of eye phenotype of rprGMR.PH

NOT Suppressor of
Statement
Reference

DreddB118 is a non-suppressor of neuroblast | larval stage phenotype of fzy1/fzy5032

DreddB118 is a non-suppressor of neuron phenotype of DroncI24, Strica4

DreddB118 is a non-suppressor of eye phenotype of AIFΔN.UAS.Tag:MYC, Scer\GAL4ey.PH

DreddB118 is a non-suppressor of wing phenotype of PGRP-LF200

DreddB118 is a non-suppressor of eye phenotype of hidGMR.PG/WGMR.PG

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The apoptosis that occurs at the interface of wild type and M(2)56FH/+ cells in M(2)56FH/+ wing discs in which wild type clones have been induced is not significantly lowered in discs that are also homozygous for DreddB118.

DreddB118 does not suppress the neuroblast loss seen in fzy5032/fzy1 mutant larval brains.

The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is strongly suppressed in dream4/DreddB118 mutants.

Triple mutants of DreddB118; dream4; NcI24 display results comparable to dream4; NcI24 double mutants, i.e. all vCrz neurons are still present having not undergone apoptosis by 7 hours after puparium formation.

The mutant eye phenotype caused by expression of AIFΔN.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey.PH is not ameliorated by DreddB118/Y.

DreddB118 does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF200 mutants.

DreddB118 dream4 double mutant females do not show any defects during oogenesis.

DreddB118; plldsRNA.Scer\UAS/+; Scer\GAL4da.G32/+ flies show similar immune response susceptibility to ROS-resistent yeast infection to DreddB118 single mutant flies.

Expression of CecA1Scer\UAS.cRa, under the control of Scer\GAL4cad-em459, ameliorates the survival rates and high intestinal microbial titers of DreddB118 flies in response to the ROS-resistant KNU53775 yeast strain and Salmonella overexpressing an antioxidant gene.

Homozygosity for DreddB118 does not supress the ablation of adult eye tissue seen in egrScer\UAS.cMa; Scer\GAL4GMR.PF animals.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (42)