Amino acid replacement: R127term.
C635067T
R105term | Dredd-PD; R105term | Dredd-PE; R105term | Dredd-PF; R51term | Dredd-PG
R127term
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.
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.
DreddB118 has abnormal immune response phenotype, non-enhanceable by Scer\GAL4da.G32/pllRNAi.UAS
DreddB118 has abnormal immune response phenotype, suppressible by CecA1UAS.cRa/Scer\GAL4cad-em459
DreddB118 is a non-enhancer of abnormal cell death phenotype of DroncI24, Strica4
DreddB118/Dredd[+] is a non-enhancer of visible phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118 is a non-enhancer of abnormal immune response phenotype of IrcRNAi.UAS, Scer\GAL4da.G32
DreddB118 is a suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpAEE5
DreddB118 is a suppressor of partially lethal - majority die phenotype of PGRP-LF200
DreddB118 is a suppressor of decreased cell death phenotype of rprGMR.PH
DreddB118/DreddB118 is a non-suppressor of FlyBase_internaltransgene_features:cell lethal:cell lethal | somatic clone phenotype of M(2)56FH
DreddB118/DreddB118 is a non-suppressor of increased cell death | somatic clone phenotype of M(2)56FH
DreddB118 is a non-suppressor of abnormal neuroanatomy | larval stage phenotype of fzy1/fzy5032
DreddB118 is a non-suppressor of decreased cell number | larval stage phenotype of fzy1/fzy5032
DreddB118 is a non-suppressor of abnormal cell death phenotype of DroncI24, Strica4
DreddB118 is a non-suppressor of visible phenotype of AIFΔN.UAS.Tag:MYC, Scer\GAL4ey.PH
DreddB118 is a non-suppressor of visible | adult stage phenotype of PGRP-LF200
DreddB118/Dredd[+] is a non-suppressor of visible phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118/Dredd[+], Strica4 has abnormal neuroanatomy | adult stage phenotype
DreddB118/Dredd[+], Strica4 has decreased cell death | adult stage phenotype
DreddB118/Dredd[+] is a non-enhancer of microchaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118/Dredd[+] is a non-enhancer of macrochaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118 is a suppressor of retina | progressive | conditional phenotype of norpAEE5
DreddB118 is a non-suppressor of neuroblast | larval stage phenotype of fzy1/fzy5032
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/Dredd[+] is a non-suppressor of microchaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118/Dredd[+] is a non-suppressor of macrochaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
DreddB118/DreddB118 is a non-suppressor of eye phenotype of Scer\GAL4GMR.PF, egrUAS.cMa
DreddB118/Dredd[+], Strica4 has peptidergic neuron | ectopic | adult stage phenotype
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; 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.