short lived | conditional (with Df(3R)ED5301)
RelE20 mutants are susceptible (show increased mortality) to infection with Ecc15 and P. burhodogranariea.
RelE20 adults show increased susceptibility (i.e. mortality) to Ecc15 and E.coli bacterial infection.
RelE20 adults show increased mortality upon infection with P. aeruginosa.
Both RelE20 homozygous (more severe) and heterozygous mutants display a strongly impaired climbing ability during adulthood (starting from a young age) while neither reveal any major disruption of the tissue or mitochondrial integrity in the flight muscles when compared to controls.
RelE20 individuals are sensitive to Ecc15 bacterial infection via feeding or septic injury.
RelE20 adults exhibit increased mortality as a result of Enterobacter cloacae infection when compared to controls.
RelE20/RelE20 flies display a decrease in both acute and chronic food intake and lipid storage in the fat body (but not intestine) compared to heterozygous controls. Resistance to starvation is significantly reduced in homozygous flies compared to both heterozygous and wild-type controls. Starved homozygous flies show a severe decrease in lipid storage and lipid droplet size.
RelE20 adults exhibit sensitivity to bacterial infection with Listeria innocua but not Erwinia carotovora.
RelE20/Df(3R)ED5301 transheterozygotes infected with DCV show a significantly decreased lifespan and a severe increase in viral load, as compared to infected controls.
Motor neurons in RelE20/RelE20 third instar larvae show a slight but significant increase in mEPSP (mini excitatory postsynaptic potential) amplitudes, no change in EPSP (excitatory postsynaptic potential) amplitude or mEPSP frequency, and a significant decrease in quantal content compared to controls. There is no difference in the number of boutons and active zones per NMJ, nor in active zone density.
RelE20 adults exhibit increased mortality upon exposure to Pseudomonas entomophila oral infection when compared to controls.
Conventionally raised and axenic (grown in antibiotics-supplemented food) RelE20 adults exhibit significantly decreased lifespan when compared to controls. Conventionally raised (but not axenic) RelE20 flies harbor more L. plantarum (but not A. pomorum) and they exhibit increased cell division in gut when compared to control adults.
RelE20 mutant adult flies exhibit increased susceptibility to Coxiella burnetii: their post-infection survival rate is significantly reduced compared to wild-type controls.
Upon repeated infection, isolated circulating naive macrophages from RelE20 larvae show a significantly decreased uptake of E.coli bacteria, as compared to equally infected controls.
RelE20 mutant flies display significantly reduced survival rate upon infection with Escherichia coli.
RelE20 mutant flies show reduced survival rate upon infection with Pseudomonas entomophila, Bacillus subtilis or Erwinia carotovora compared to wild-type.
The sensitivity of RelE20 mutants to radiation is comparable to wild-type controls as their eclosion rate following irradiation during third larval instar is not significantly affected.
RelE20 adult mutant flies show significantly lower survival rate upon infection with Gram-negative bacteria compared to controls.
Mutant adults show reduced survival compared to wild type after septic injury with Gram negative bacteria (either Salmonella typhimurium or Enterobacter cloacae).
In contrast to wild-type, survival of RelE20 mutant flies is compromised following Erwinia carotovora Ecc15 infection.
RelE20 mutant flies exposed to non-replicating P. aeruginosa bacteria display the same survival rate as non-exposed flies. Wild-type flies exhibit a greater survival rate due to a build up of immunity.
Mutant flies show reduced compared to wild type after injection with Ecc15 (Gram-negative bacterium).
Median survival in days is reduced in mutant flies compared to wild type.
Intestinal stem cell proliferation is increased in RelE20 mutants.
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.
RelE20 mutant flies show higher levels of viral replication and viral titers 5 days after intrathoracic infection with 200 pfu of Sindbis virus compared to controls.
Short term starvation improves the survival and containment of infection of RelE20 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 RelE20 mutants.
Infection with either gram-negative or gram-positive pathogens results in between 80-90% levels of death in RelE20 mutants. Short term starvation (STS)improves the survival rate considerably, with only 40% of STS flies dying in the same period.
RelE20 mutant flies, infected by septic injury with a needle dipped in E. carotovora quickly succumb to the infection, whereas wild-type flies survive.
RelE20 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.
RelE20 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 RelE20 and wild-type flies. However, upon dissection 24 hours after genital infection, bacteria are found in the body cavity of 19% of RelE20 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 RelE20 flies. Mortality is observed in wild-type, and more strongly in RelE20 flies after genital infection with a strain of Pseudomonas aeruginosa.
RelE20 flies have a reduced survival time compared to controls following challenge with the gram-negative bacteria Erwinia carotovora 15 (Ecc15).
RelE20 mutants are highly sensitive to Gram-negative bacterial infection.
RelE20 flies show significantly lower survival rates compared to control flies after infection with E.cloacae by septic injury.
RelE20 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. RelE20 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. RelE20 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.
RelE20 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.
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 show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).
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).
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.
RelE20 has abnormal neurophysiology | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
RelE20 has visible | dominant phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has abnormal immune response phenotype, enhanceable by spz4
RelE20 has abnormal immune response phenotype, enhanceable by Tlr3/Tlrv1
RelE20 has short lived | nutrition conditional phenotype, non-enhanceable by TrpA1ins
RelE20, spz4 has short lived | conditional phenotype, suppressible | partially by BaraA1UAS.cHa/Scer\GAL4Act5C.PI
RelE20, spz4 has abnormal immune response | adult stage phenotype, suppressible | partially by BaraA1UAS.cHa/Scer\GAL4Act5C.PI
RelE20 has abnormal starvation stress response | recessive | adult stage phenotype, suppressible by foxoW24/foxo[+]
RelE20 has abnormal starvation stress response | recessive | adult stage phenotype, suppressible by Scer\GAL4Cg.PA/foxoKK108485
RelE20 has abnormal immune response phenotype, non-suppressible by edinUAS.cVa/Scer\GAL4c564
RelE20/RelE20 is an enhancer of abnormal locomotor behavior | adult stage phenotype of Pink1B9
RelE20 is an enhancer of neoplasia | larval stage phenotype of dlg1A40.2
RelE20/Rel[+] is an enhancer of visible | dominant phenotype of DreddEP1412
RelE20 is an enhancer of abnormal immune response phenotype of spz4
RelE20/Rel[+] is a non-enhancer of abnormal locomotor behavior | adult stage phenotype of Pink1B9
RelE20 is a non-enhancer of radiation sensitive phenotype of spz4
RelE20 is a suppressor of increased cell death | larval stage phenotype of dlg1A40.2
RelE20 is a suppressor | partially of abnormal immune response phenotype of TrpA1ins
RelE20/Df(3R)ED5331 is a suppressor of abnormal neuroanatomy | recessive | adult stage | progressive phenotype of dnr12-133
RelE38/RelE20 is a suppressor of abnormal neuroanatomy | recessive | adult stage | progressive phenotype of dnr12-133
RelE20 is a suppressor of increased cell death | semidominant | adult stage phenotype of tefuatm-8
RelE20 is a suppressor of short lived phenotype of tefuatm-8
RelE20 is a suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpAEE5
RelE38/RelE20 is a suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpAEE5
RelE20 is a suppressor of partially lethal - majority die phenotype of PGRP-LF200
RelE20, Scer\GAL4S106-GS is a suppressor of abnormal immune response phenotype of PGRP-LEUAS.Tag:FLAG, Scer\GAL4S106-GS
RelE20/Rel[+] is a non-suppressor of abnormal locomotor behavior | adult stage phenotype of Pink1B9
RelE20/RelE20 is a non-suppressor of abnormal immune response | recessive | adult stage phenotype of ClC-b1
PGRP-LEUAS.Tag:FLAG/Scer\GAL4He.PZ, RelE20/RelE20 is a non-suppressor of abnormal immune response | recessive | adult stage phenotype of ClC-b1
RelE20 is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg61
RelE20/Dif1 is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg61
RelE20, Df(2L)J4, Dif1 is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg61
RelE20 is a non-suppressor of visible | adult stage phenotype of PGRP-LF200
RelE20, spz4 has short lived | conditional phenotype
RelE20, spz4 has abnormal immune response | adult stage phenotype
RelE20, foxoW24 has partially lethal - majority die | recessive phenotype
RelE20, foxoW24 has majority die during P-stage | recessive phenotype
RelE20, brm[+]/brm2 has abnormal immune response phenotype
RelE20, brm[+]/brm2 has short lived | conditional phenotype
RelE20, mor[+]/mor1 has abnormal immune response phenotype
RelE20, mor[+]/mor1 has short lived | conditional phenotype
PGRP-LBΔ/Df(2R)PGRP-SCΔ, RelE20, pirkEY00723 has long lived phenotype
RelE20/Rel[+], keyc02831 has abnormal immune response | dominant phenotype
RelE20/Rel[+], IKKβF22 has abnormal immune response | dominant phenotype
Dif1, RelE20 has decreased body size phenotype
Dif1, RelE20 has partially lethal - majority die | larval stage phenotype
RelE20, dl1 has decreased body size phenotype
RelE20, dl1 has partially lethal - majority die | larval stage phenotype
RelE20, imd1 has abnormal immune response phenotype
RelE20 has abdominal segment motor neuron | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
RelE20 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16
RelE20 has mesothoracic tergum phenotype, enhanceable by scHw-Ua
RelE20 has macrochaeta | ectopic phenotype, enhanceable by scHw-Ua
RelE20 has mesothoracic tergum phenotype, enhanceable by Tollo1/Tollo[+]
RelE20 has macrochaeta | ectopic phenotype, enhanceable by Tollo1/Tollo[+]
RelE20 has mesothoracic tergum phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has macrochaeta | ectopic phenotype, enhanceable by Dredd[+]/DreddEP1412
RelE20 has adult fat body | nutrition conditional phenotype, suppressible by foxoW24/foxo[+]
RelE20 has adult fat body | nutrition conditional phenotype, suppressible by Scer\GAL4Cg.PA/foxoKK108485
RelE20 has adult fat body | nutrition conditional phenotype, suppressible by bmmGD5139/Scer\GAL4Cg.PA
RelE20/Rel[+] is an enhancer of eye phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, egrUAS.cMa
RelE20/Rel[+] is an enhancer of phenotype of Zzzz\repScer\UAS.T:Avic\GFP/Sindbis\repUAS.GFP
RelE20 is an enhancer of macrochaeta | ectopic phenotype of scHw-Ua
RelE20 is an enhancer of mesothoracic tergum phenotype of scHw-Ua
RelE20/Rel[+] is an enhancer of mesothoracic tergum phenotype of Tollo1
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 macrochaeta | ectopic phenotype of DreddEP1412
RelE20/Rel[+] is a non-enhancer of flight muscle cell phenotype of Pink1B9
RelE20/Rel[+] is a non-enhancer of mitochondrion | adult stage phenotype of Pink1B9
RelE20/RelE20 is a non-enhancer of flight muscle cell phenotype of Pink1B9
RelE20/RelE20 is a non-enhancer of mitochondrion | adult stage phenotype of Pink1B9
RelE20/Df(3R)ED5331 is a suppressor of adult brain | progressive phenotype of dnr12-133
RelE38/RelE20 is a suppressor of adult brain | progressive phenotype of dnr12-133
RelE20 is a suppressor of retina | progressive | conditional phenotype of norpAEE5
RelE38/RelE20 is a suppressor of retina | progressive | conditional phenotype of norpAEE5
RelE20/Rel[+] is a non-suppressor of flight muscle cell phenotype of Pink1B9
RelE20/Rel[+] is a non-suppressor of mitochondrion | adult stage phenotype of Pink1B9
RelE20/RelE20 is a non-suppressor of flight muscle cell phenotype of Pink1B9
RelE20/RelE20 is a non-suppressor of mitochondrion | adult stage phenotype of Pink1B9
RelE20 is a non-suppressor of wing phenotype of PGRP-LF200
RelE20 heterozygous mutation does not modify the impaired climbing ability or the disrupted tissue or mitochondrial integrity in the flight
muscles phenotype of young Pink1B9 mutants.
RelE20 homozygous mutation enhances the impaired climbing ability phenotype of young Pink1B9 mutants while it does not modify disrupted tissue or mitochondrial integrity in the flight muscles phenotype of young Pink1B9 mutants.
Motor neurons in RelE20, GluRIIASP16 double mutant third instar larvae have further reduced mEPSP (mini excitatory postsynaptic potential) compared to single RelE20 (but not GluRIIASP16) mutants; reduced EPSP (excitatory postsynaptic potential) amplitudes compared to either single mutant; and reduced quantal content compared to single GluRIIASP16 (but not RelE20) mutants. Their capacity for long-term presynaptic homeostatic plasticity (i.e. increase in quantal content causing an increase in EPSP amplitude, approaching baseline) is completely blocked.
RelE20 fails to suppress the melanotic mass phenotype seen in Atg61 mutant third instar larvae.
A Dif1 RelE20 double mutant background fails to suppress the melanotic mass phenotype seen in Atg61 mutant third instar larvae.
A Dif1/Df(2L)J4 RelE20 mutant background fails to suppress the melanotic mass phenotype seen in Atg61 mutant third instar larvae.
Expression of edinScer\UAS.cVa under the control of Scer\GAL4c564 does not suppress the reduced survival of RelE20 flies after infection by E. cloacae.
pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ, RelE20 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 pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ flies.
A RelE20 heterozygous background suppresses POSH mediated cell survival, resulting in reduced eye size in flies overexpressing POSHScer\UAS.cSa and egrScer\UAS.cMa in the developing eye disc under the control of Scer\GAL4GMR.PF.
keyc02831/+ ; RelE20/+ 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).
ird5F22/+ ; RelE20/+ double heterozygotes are more sensitive to Cricket Paralysis virus infection (after being injected with the virus) than control flies.
RelE20 does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF200 mutants.
RelE20/+ Tollo1/+ double heterozygotes show ectopic bristles in 55% of heminota at 18[o]C, a significant enhancement compared to the single heterozygotes.
DreddEP1412/+ RelE20/+ double heterozygotes show ectopic bristles in 58% of heminota at 18[o]C, a significant enhancement compared to the single heterozygotes.
scHw-Ua RelE20 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 JraIA109 heterozygous flies after infection with E.coli is suppressed if the flies are also heterozygous for RelE20.
The lower survival rate seen in Dsp1EP355 mutant flies after infection with E.coli is suppressed if the flies are also heterozygous for RelE20.
The lower survival rate seen in flies expressing Stat92EdsRNA.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\GAL4da.G32 driver to drive expression) after infection with E.coli is suppressed if the flies are also heterozygous for RelE20.
The enhanced pathogen resistance phenotype of flies expressing PGRP-LEScer\UAS.T:Zzzz\FLAG driven by Scer\GAL4S106-GS is completely suppressed by homozygous RelE20.
RelE20, imd1 double mutant animals are equally susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
Heterozygosity for RelE20 in a Scer\GAL4Act5C.PI Zzzz\repScer\UAS.T:Avic\GFP background results in increased Sindbis viral replication.
RelE20 is rescued by RelUAS.Tag:polyHis/Scer\GAL4hs.PB
RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4Cg.PA
RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4Cg.PA
RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4c564
RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4cad-em459
Expressing RelUAS.Tag:polyHis under the control of Scer\GAL4Cg.PA fully rescues lipid storage defects and only partially rescues the reduced resistance to starvation in RelE20/RelE20 adults.
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.
Induced with: NmdmcE20.