A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\RelE20

General Information
SymbolDmel\RelE20SpeciesD. melanogaster
NameFlyBase IDFBal0101572
Feature typealleleAssociated geneDmel\Rel
Also Known AsRelishE20
Allele classloss of function allele
MutagenDelta2-3
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
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Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Imprecise excision of the P{lacW} element, removing all four Rel transcription start sites.
Cytology
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Statement
Reference
Mutant flies show greatly reduced survival compared to wild type after septic injury with Erwinia carotovora carotovora 15.
Mutant flies show severely reduced survival in response to infection with E. coli/
Homozygous larvae have reduced levels of triacylglycerols compared to wild type.
Mutant flies are sensitive to infection with E. cloacae, showing reduced survival after infection compared to the survival of wild-type controls.
Mutant flies show a reduced survival rate compared to control flies after infection with either E.coli or P. aeruginosa. The mutant flies show normal resistance to infection with either S. aureus or A. fumigatus.
Short term starvation improves the survival and containment of infection of Rel[E20] mutant flies following immune challenge with Gram-negative bacteria. Administering the NO Synthase-inhibitory arginine analog N-Nitro-L-Arginine- Methyl-Ester (L-NAME) but not its inactive enantiomer D-NAME, increased sensitivity to infection once again to levels expected for Rel[E20] mutants. Infection with either gram-negative or gram-positive pathogens results in between 80-90% levels of death in Rel[E20] mutants. Short term starvation (STS)improves the survival rate considerably, with only 40% of STS flies dying in the same period.
Rel[E20] mutant flies, infected by septic injury with a needle dipped in E. carotovora quickly succumb to the infection, whereas wild-type flies survive. Rel[E20] mutant flies, infected by septic injury with a needle dipped in L. monocytogenes quickly succumb to the infection, whereas wild-type flies survive.
Homozygous flies are more sensitive to Cricket Paralysis virus infection (after being injected with the virus) than control flies.
Rel[E20] flies display an increase in susceptibility and mortality to genital infection (and subsequent infection throughout the body) compared to wild-type controls. There is no apparent difference between E.carotova infection on the outside of the genitalia in Rel[E20] and wild-type flies. However, upon dissection 24 hours after genital infection, bacteria are found in the body cavity of 19% of Rel[E20] mutant flies, while no bacteria are found inside wild-type flies. Consistent with this, there is a weak but significant mortality after genital infection in Rel[E20] flies. Mortality is observed in wild-type, and more strongly in Rel[E20] flies after genital infection with a strain of Pseudomonas aeruginosa.
Rel[E20] flies have a reduced survival time compared to controls following challenge with the gram-negative bacteria Erwinia carotovora 15 (Ecc15).
Rel[E20] flies show a normal lifespan on dead yeast medium and on live yeast medium. Rel[E20] flies have a low number of living yeast in the gut (assayed as the number of colony-forming units from homogenates of surface-sterilized intestines), as do wild-type flies.
RelE20 mutants are highly sensitive to Gram-negative bacterial infection.
Rel[E20] flies show significantly lower survival rates compared to control flies after infection with E.cloacae by septic injury.
Rel[E20] mutants show 98% lethality one month after infection with a 1:1 mixture of M. luteus and E.coli, compared to 10% in wild-type. Rel[E20] mutant adults are more sensitive to fungal infection than wild type flies, with 100% lethality at 22 days. This compares to only 55-70% at 30 days in wild type. Rel[E20] mutant larvae show a reduced eclosion rate following injection with M. luteus and E. coli.
Homozygous flies show ectopic macrochaetae in 38% of heminota analysed at 18[o]C (this phenotype is not seen at 25[o]C). In most cases, one ectopic macrochaeta is seen per heminotum. Heterozygous flies show ectopic dorsocentral bristles in the medial notum in 26% of heminota at 18[o]C.
Mutant flies are defective clearing bacteria after injection with E.coli.
Homozygous virgin females have significantly higher bacterial counts per fly after infection with S.marcescens compared to their sibling control females.
Mutant flies show reduced survival compared to control flies after infection with E.coli, but show normal levels of survival after infection with A.fumigatus.
RelE20 flies exhibit a dramatically decreased viability when pricked with a needle dipped in a concentrated solution of gram-negative Esherichia coli or Erwinia carotovora.
Rel[E20] mutant flies are highly susceptible to infection by gram-negative bacteria, and the majority of flies die within 25 hours of septic injury.
High mortality levels are observed when RelE20 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. RelE20 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 strain when it does not overexpress the antioxidant gene. Infection of RelE20 flies with an Escherichia coli strain that overexpresses an antioxidant gene leads to host death following severe damage to epithelial cells. Following infection, the midgut of these flies becomes visibly swollen, there is a morphological alteration of its columnar structure and epithelial cells degenerate. Although the visceral musculature appears to remain intact, intestinal cells adopt a flat morphology. This pathology is not seen in controls.
Mutant flies show reduced survival rates compared to control flies after bacterial (E.carotovora) infection.
Mutant animals, like wild-type, are significantly less susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
RelE20 flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).
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.
RelE20 flies are more susceptible to Psuedomonas entomophila infection that wild-type flies, with both larvae and adults RelE20 flies succumbing faster to infection than wild-type flies.
RelE20 flies exhibit no significant altered sensitivity to viral infection compared to wild-type.
RelE20 flies are susceptible to infection by Gram-negative bacteria (P.carotovorum.carotovorum).
Mutants show no detectable induction of Dpt, CecA1 and CecA2. Attacin levels are reduced compared to wild type and Drs induction is normal.
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.
Mutant flies show the same level of resistance to B.bassiana (when their cuticles are coated with spores) as wild-type flies.
RelE20 flies do not survive injection with E.cloacae β12 (injection with approximately 2 x 105 bacteria per fly), dying within 17 hours, in contrast to wild-type flies. Lower doses of bacteria also kill the mutant flies (even at an average estimated dose of 0.2 bacteria per fly). The flies are more sensitive to injection with the fungi G.candidum, D.uninucleata or M.anisopliae than wild-type flies, the majority of mutant flies being killed within a week. Larvae show an efficient encapsulation reaction when infested with the parasitoid wasp L.boulardi. Total hemocyte cell number and morphology appears normal and the lymph glands are also not visibly affected. The phagocytic activity of hemocytes after injection with bacteria is indistinguishable from wild type.
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Statement
Reference
RelE20 has visible | dominant phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has visible | dominant phenotype, enhanceable by Tollo1/Tollo[+]
RelE20 has visible phenotype, enhanceable by scHw-Ua
hideNOT suppressed by
Statement
Reference
hideEnhancer of
Statement
Reference
RelE20/Rel[+] is an enhancer of visible | dominant phenotype of DreddEP1412
RelE20/Rel[+] is an enhancer of visible | dominant phenotype of Tollo1
RelE20 is an enhancer of visible phenotype of scHw-Ua
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Statement
Reference
RelE20/Rel[+] is a suppressor | partially of lethal phenotype of Atf376
hideNOT Suppressor of
Statement
Reference
RelE20 is a non-suppressor of visible | adult stage phenotype of PGRP-LF200
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Statement
Reference
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Statement
Reference
RelE20 has macrochaeta | ectopic phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has macrochaeta | ectopic phenotype, enhanceable by scHw-Ua
RelE20 has macrochaeta | ectopic phenotype, enhanceable by Tollo1/Tollo[+]
RelE20 has mesothoracic tergum phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has mesothoracic tergum phenotype, enhanceable by scHw-Ua
RelE20 has mesothoracic tergum phenotype, enhanceable by Tollo1/Tollo[+]
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Statement
Reference
RelE20/Rel[+] is an enhancer of macrochaeta | ectopic phenotype of DreddEP1412
RelE20/Rel[+] is an enhancer of macrochaeta | ectopic phenotype of Tollo1
RelE20/Rel[+] is an enhancer of mesothoracic tergum phenotype of DreddEP1412
RelE20/Rel[+] is an enhancer of mesothoracic tergum phenotype of Tollo1
RelE20 is an enhancer of macrochaeta | ectopic phenotype of scHw-Ua
RelE20 is an enhancer of mesothoracic tergum phenotype of scHw-Ua
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Statement
Reference
RelE20 is a non-suppressor of wing phenotype of PGRP-LF200
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Statement
Reference
The increased levels of triacylglycerols and diacylglycerols which are seen in Atf3[76] larvae are reduced if the larvae are also heterozygous for Rel[E20]. In addition, heterozygosity for Rel[E20] also reduces the increased levels of free fatty acids seen in Atf3[76] larvae.
Expression of edin[Scer\UAS.cVa] under the control of Scer\GAL4[c564] does not suppress the reduced survival of Rel[E20] flies after infection by E. cloacae.
pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ], Rel[E20] flies, with impaired imd pathway activity due to the presence of Dredd or Rel mutations, exhibit an increased lifespan upon oral infection with E. carotovora bacteria, compared to pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies.
A Rel[E20] heterozygous background suppresses POSH mediated cell survival, resulting in reduced eye size in flies overexpressing POSH[Scer\UAS.cSa] and egr[Scer\UAS.cMa] in the developing eye disc under the control of Scer\GAL4[GMR.PF].
key[c02831]/+ ; Rel[E20]/+ double heterozygotes are more sensitive to Cricket Paralysis virus infection (after being injected with the virus) than control flies (neither single heterozygote shows increased sensitivity to Cricket Paralysis virus infection). ird5[F22]/+ ; Rel[E20]/+ double heterozygotes are more sensitive to Cricket Paralysis virus infection (after being injected with the virus) than control flies.
Rel[E20] does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF[200] mutants.
Rel[E20]/+ Tollo[1]/+ double heterozygotes show ectopic bristles in 55% of heminota at 18[o]C, a significant enhancement compared to the single heterozygotes. Dredd[EP1412]/+ Rel[E20]/+ double heterozygotes show ectopic bristles in 58% of heminota at 18[o]C, a significant enhancement compared to the single heterozygotes. sc[Hw-Ua] Rel[E20] flies show one ectopic macrochaeta in 13% of heminota more than one ectopic macrochaeta in 85% of heminota analysed at 18[o]C.
The lower survival rate seen in Jra[IA109] heterozygous flies after infection with E.coli is suppressed if the flies are also heterozygous for Rel[E20]. The lower survival rate seen in Dsp1[EP355] mutant flies after infection with E.coli is suppressed if the flies are also heterozygous for Rel[E20]. The lower survival rate seen in flies expressing Stat92E[dsRNA.Scer\UAS] (either using heat shock to drive expression from the minimal heat shock promoter in the P{UAS-Stat92E.RNAi} construct, or using a Scer\GAL4[da.G32] driver to drive expression) after infection with E.coli is suppressed if the flies are also heterozygous for Rel[E20].
The enhanced pathogen resistance phenotype of flies expressing PGRP-LE[Scer\UAS.T:Zzzz\FLAG] driven by Scer\GAL4[S106-GS] is completely suppressed by homozygous Rel[E20].
RelE20 Dif1 double mutant larvae are smaller than wild-type, and about half of the double homozygotes die before reaching adult stages. RelE20 dl1 double mutant larvae are smaller than wild-type, and about half of the double homozygotes die before reaching adult stages.
RelE20, imd1 double mutant animals are equally susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
The addition of spz4 or Tlrv1/Tlr3 enhances the susceptibility of RelE20 mutants to E.coli and M.luteus infection.
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Fails to complement
Rescued by
Partially rescued by
Comments
Expression of RelScer\UAS.T:Zzzz\His6 in the intestine, driven by Scer\GAL4cad-em459, results in the increased survival rate of RelE20 flies to control levels following infection with the ROS-resistant KNU53775 yeast strain. However, expression of RelScer\UAS.T:Zzzz\His6 in the fat body, driven by Scer\GAL4c564, does not increase the survival rates of RelE20 flies following KNU53775 infection. In contrast, expression of RelScer\UAS.T:Zzzz\His6 increases survival rates of RelE20 flies in response to infection with Erwinia carotovora carotovora 15 when driven by Scer\GAL4c564 but does not increase survival when driven with Scer\GAL4cad-em459.
RelScer\UAS.T:Zzzz\His6 rescues the immune defects of RelE20 flies when expressed under the control of Scer\GAL4hs.PB.
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Bloomington
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hide Recent research papers ( 14 )
Bosco-Drayon et al., 2012, Cell Host Microbe 12(2): 153--165
Peptidoglycan Sensing by the Receptor PGRP-LE in the Drosophila Gut Induces Immune Responses to Infectious Bacteria and Tolerance to Microbiota. [FBrf0219236]
Meinander et al., 2012, EMBO J. 31(12): 2770--2783
Ubiquitylation of the initiator caspase DREDD is required for innate immune signalling. [FBrf0218688]
Overend et al., 2012, Peptides 34(1): 209--218
The receptor guanylate cyclase Gyc76C and a peptide ligand, NPLP1-VQQ, modulate the innate immune IMD pathway in response to salt stress. [FBrf0217783]
Rynes et al., 2012, Mol. Cell. Biol. 32(19): 3949--3962
Activating transcription factor 3 regulates immune and metabolic homeostasis. [FBrf0219385]
Tsuzuki et al., 2012, Sci. Rep. 2: 210
Drosophila growth-blocking peptide-like factor mediates acute immune reactions during infectious and non-infectious stress. [FBrf0217467]
Vanha-Aho et al., 2012, PLoS ONE 7(5): e37153
Functional Characterization of the Infection-Inducible Peptide Edin in Drosophila melanogaster. [FBrf0218357]
Wang et al., 2012, J. Immunol. 188(8): 3993--4000
The Drosophila protein mustard tailors the innate immune response activated by the immune deficiency pathway. [FBrf0217978]
Akhouayri et al., 2011, PLoS Pathog. 7(10): e1002319
Toll-8/tollo negatively regulates antimicrobial response in the Drosophila respiratory epithelium. [FBrf0216452]
Clark et al., 2011, Curr. Biol. 21(19): 1672--1677
Multiple TGF-β Superfamily Signals Modulate the Adult Drosophila Immune Response. [FBrf0216429]
Fullaondo et al., 2011, Mol. Cell. Biol. 31(14): 2960--2972
Spn1 Regulates the GNBP3-Dependent Toll Signaling Pathway in Drosophila melanogaster. [FBrf0214037]
Narbonne-Reveau et al., 2011, PLoS ONE 6(2): e17470
Lack of an antibacterial response defect in Drosophila toll-9 mutant. [FBrf0213211]
Paredes et al., 2011, Immunity 35(5): 770--779
Negative Regulation by Amidase PGRPs Shapes the Drosophila Antibacterial Response and Protects the Fly from Innocuous Infection. [FBrf0216727]
van Uden et al., 2011, PLoS Genet. 7(1): e1001285
Evolutionary Conserved Regulation of HIF-1β by NF-κB. [FBrf0212948]
Zaidman-Rémy et al., 2011, PLoS ONE 6(2): e17231
Drosophila Immunity: Analysis of PGRP-SB1 Expression, Enzymatic Activity and Function. [FBrf0213192]