FB2021_02, released April 13, 2021

Allele: Dmel\RelE20

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General Information
Symbol
Dmel\RelE20
Species
D. melanogaster
Name
FlyBase ID
FBal0101572
Feature type
allele
Associated gene
Dmel\Rel
Associated Insertion(s)
Carried in Construct
Also Known As
RelishE20, RelE20
Key Links
Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Kambris et al., 2006)
Mutagen
Delta2-3 transposase
(Hedengren et al., 1999)
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
AF186076
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
       
      Progenitor genotype
      RelL3141a
      (Hedengren, 1999.9.14, Hedengren et al., 1999)
      Cytology
      Nature of the lesion
      Statement
      Reference

      Imprecise excision of the P{lacW} element, removing all four Rel transcription start sites.

      (Hedengren et al., 1999)
      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
      ameliorates  neurodegenerative disease
      modeled by tefuatm-8
      (Petersen et al., 2013)
      ameliorates  retinal disease
      modeled by norpA7
      (Chinchore et al., 2012)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class

      abnormal feeding behavior | adult stage | recessive

      (Molaei et al., 2019)

      abnormal immune response

      (Du et al., 2016, Binggeli et al., 2014, Bonnay et al., 2014, Gendrin et al., 2013, Meinander et al., 2012, Overend et al., 2012, Vanha-Aho et al., 2012, Chen et al., 2010, Avadhanula et al., 2009, Buchon et al., 2009, Costa et al., 2009, Gendrin et al., 2009, Geuking et al., 2009, Kleino et al., 2008, Ratnaparkhi et al., 2008, Kim et al., 2007, Mueller et al., 2007, Brun et al., 2006, Kim et al., 2006, Leulier et al., 2006, Ryu et al., 2006, Tang et al., 2006, Vodovar et al., 2005, Lu et al., 2001, Leulier et al., 2000, Hedengren et al., 1999)

      abnormal immune response (with Df(3R)ED5301)

      (Goto et al., 2018)

      abnormal immune response | adult stage

      (Aalto et al., 2019, Lin et al., 2019, Parvy et al., 2019, Iatsenko et al., 2018, Bastos et al., 2017, Asaoka et al., 2016, Iatsenko et al., 2016, Morris et al., 2016, Xiao et al., 2015, Goto et al., 2008)

      abnormal immune response | adult stage | recessive

      (Wong et al., 2017, Brown et al., 2009)

      abnormal locomotor behavior | adult stage

      (Lee et al., 2020)

      abnormal locomotor behavior | adult stage | dominant

      (Lee et al., 2020)

      abnormal neurophysiology | third instar larval stage

      (Harris et al., 2018)

      abnormal size | adult stage | recessive | nutrition conditional

      (Molaei et al., 2019)

      abnormal starvation stress response | adult stage | recessive

      (Molaei et al., 2019)

      increased mortality | adult stage

      (Lin et al., 2019, Iatsenko et al., 2018)

      increased occurrence of cell division | adult stage

      (Iatsenko et al., 2018, Wang et al., 2013)

      short lived

      (Iatsenko et al., 2018, Petersen et al., 2013)

      short lived | conditional

      (Aalto et al., 2019, Parvy et al., 2019, Morris et al., 2016, Bonnay et al., 2014)

      short lived | conditional (with Df(3R)ED5301)

      (Goto et al., 2018)

      short lived | nutrition conditional

      (Du et al., 2016)

      viable

      (Molaei et al., 2019, Lehmann et al., 2002)

      visible | cold sensitive

      (Ayyar et al., 2007)

      visible | dominant

      (Ayyar et al., 2007)
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      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.

      (Lee et al., 2020)

      RelE20 individuals are sensitive to Ecc15 bacterial infection via feeding or septic injury.

      (Aalto et al., 2019)

      RelE20 adults exhibit increased mortality as a result of Enterobacter cloacae infection when compared to controls.

      (Lin et al., 2019)

      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.

      (Molaei et al., 2019)

      RelE20 adults exhibit sensitivity to bacterial infection with Listeria innocua but not Erwinia carotovora.

      (Parvy et al., 2019)

      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.

      (Goto et al., 2018)

      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.

      (Harris et al., 2018)

      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.

      (Iatsenko et al., 2018)

      RelE20 mutant adult flies exhibit increased susceptibility to Coxiella burnetii: their post-infection survival rate is significantly reduced compared to wild-type controls.

      (Bastos et al., 2017)

      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.

      (Wong et al., 2017)

      RelE20 mutant flies display significantly reduced survival rate upon infection with Escherichia coli.

      (Asaoka et al., 2016)

      RelE20 mutants show normal uracil-dependent defecation.

      Guts from RelE20 mutants exhibited a decrease in colony-forming units 5 and 8 hours after feeding with the microbe Erwinia carotovora.

      When fed Erwinia carotovora, RelE20 mutants display a significantly higher mortality rate than control flies.

      (Du et al., 2016)

      RelE20 mutant flies show reduced survival rate upon infection with Pseudomonas entomophila, Bacillus subtilis or Erwinia carotovora compared to wild-type.

      (Iatsenko et al., 2016)

      RelE20/RelE20 mutants exhibit a significant decrease in survival in response to P. rettgeri or L. monocytogenes infection, as compared to wild type.

      (Morris et al., 2016)

      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.

      (Sudmeier et al., 2015)

      RelE20 adult mutant flies show significantly lower survival rate upon infection with Gram-negative bacteria compared to controls.

      (Xiao et al., 2015)

      Mutant adults show reduced survival compared to wild type after septic injury with Gram negative bacteria (either Salmonella typhimurium or Enterobacter cloacae).

      (Binggeli et al., 2014)

      In contrast to wild-type, survival of RelE20 mutant flies is compromised following Erwinia carotovora Ecc15 infection.

      (Bonnay et al., 2014)

      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.

      (Christofi and Apidianakis, 2013)

      Mutant flies show reduced compared to wild type after injection with Ecc15 (Gram-negative bacterium).

      (Gendrin et al., 2013)

      Median survival in days is reduced in mutant flies compared to wild type.

      (Petersen et al., 2013)

      Intestinal stem cell proliferation is increased in RelE20 mutants.

      (Wang et al., 2013)

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

      (Meinander et al., 2012)

      Mutant flies show severely reduced survival in response to infection with E. coli/

      (Overend et al., 2012)

      Homozygous larvae have reduced levels of triacylglycerols compared to wild type.

      (Rynes et al., 2012)

      Mutant flies are sensitive to infection with E. cloacae, showing reduced survival after infection compared to the survival of wild-type controls.

      (Vanha-Aho et al., 2012)

      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.

      (Chen et al., 2010)

      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.

      (Avadhanula et al., 2009)

      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.

      (Brown et al., 2009)

      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.

      (Buchon et al., 2009)

      Homozygous flies are more sensitive to Cricket Paralysis virus infection (after being injected with the virus) than control flies.

      (Costa et al., 2009)

      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.

      (Gendrin et al., 2009)

      RelE20 flies have a reduced survival time compared to controls following challenge with the gram-negative bacteria Erwinia carotovora 15 (Ecc15).

      (Geuking et al., 2009)

      RelE20 flies show a normal lifespan on dead yeast medium and on live yeast medium. RelE20 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.

      (Ha et al., 2009)

      RelE20 mutants are highly sensitive to Gram-negative bacterial infection.

      (Goto et al., 2008)

      RelE20 flies show significantly lower survival rates compared to control flies after infection with E.cloacae by septic injury.

      (Kleino et al., 2008)

      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.

      (Ratnaparkhi et al., 2008)

      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.

      (Ayyar et al., 2007)

      Mutant flies are defective clearing bacteria after injection with E.coli.

      (Kim et al., 2007)

      Homozygous virgin females have significantly higher bacterial counts per fly after infection with S.marcescens compared to their sibling control females.

      (Mueller et al., 2007)

      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.

      (Brun et al., 2006)

      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.

      (Kim et al., 2006)

      RelE20 mutant flies are highly susceptible to infection by gram-negative bacteria, and the majority of flies die within 25 hours of septic injury.

      (Leulier et al., 2006)

      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.

      (Ryu et al., 2006)

      Mutant flies show reduced survival rates compared to control flies after bacterial (E.carotovora) infection.

      (Tang et al., 2006)

      Mutant animals, like wild-type, are significantly less susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.

      (Apidianakis et al., 2005)

      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.

      (Ha et al., 2005)

      RelE20 flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).

      (Ha et al., 2005)

      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.

      (Vodovar et al., 2005)

      RelE20 flies exhibit no significant altered sensitivity to viral infection compared to wild-type.

      (Zambon et al., 2005)

      RelE20 flies are susceptible to infection by Gram-negative bacteria (P.carotovorum.carotovorum).

      (Pili-Floury et al., 2004)

      Mutants show no detectable induction of Dpt, CecA1 and CecA2. Attacin levels are reduced compared to wild type and Drs induction is normal.

      (Lu et al., 2001)

      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.

      (Leulier et al., 2000)

      Mutant flies show the same level of resistance to B.bassiana (when their cuticles are coated with spores) as wild-type flies.

      (Rutschmann et al., 2000)

      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.

      (Hedengren et al., 1999)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      RelE20 has abnormal neurophysiology | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16

      (Harris et al., 2018)

      RelE20 has visible phenotype, enhanceable by scHw-Ua

      (Ayyar et al., 2007)

      RelE20 has visible | dominant phenotype, enhanceable by Tollo1/Tollo[+]

      (Ayyar et al., 2007)

      RelE20 has visible | dominant phenotype, enhanceable by Dredd[+]/DreddEP1412

      (Ayyar et al., 2007)

      RelE20 has abnormal immune response phenotype, enhanceable by spz4

      (De Gregorio et al., 2002)

      RelE20 has abnormal immune response phenotype, enhanceable by Tlr3/Tlrv1

      (De Gregorio et al., 2002)
      NOT Enhanced by
      Statement
      Reference

      RelE20 has short lived | nutrition conditional phenotype, non-enhanceable by TrpA1ins

      (Du et al., 2016)
      Suppressed by
      NOT suppressed by
      Statement
      Reference

      RelE20 has abnormal immune response phenotype, non-suppressible by edinUAS.cVa/Scer\GAL4c564

      (Vanha-Aho et al., 2012)
      Enhancer of
      Statement
      Reference

      RelE20/RelE20 is an enhancer of abnormal locomotor behavior | adult stage phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20 is an enhancer of neoplasia | larval stage phenotype of dlg1A40.2

      (Parvy et al., 2019)

      RelE20 is an enhancer of visible phenotype of scHw-Ua

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of visible | dominant phenotype of Tollo1

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of visible | dominant phenotype of DreddEP1412

      (Ayyar et al., 2007)

      RelE20 is an enhancer of abnormal immune response phenotype of spz4

      (De Gregorio et al., 2002)
      NOT Enhancer of
      Statement
      Reference

      RelE20/Rel[+] is a non-enhancer of abnormal locomotor behavior | adult stage phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20 is a non-enhancer of radiation sensitive phenotype of spz4

      (Sudmeier et al., 2015)
      Suppressor of
      NOT Suppressor of
      Other
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      RelE20 has abdominal segment motor neuron | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16

      (Harris et al., 2018)

      RelE20 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, enhanceable by GluRIIASP16/GluRIIASP16

      (Harris et al., 2018)

      RelE20 has mesothoracic tergum phenotype, enhanceable by scHw-Ua

      (Ayyar et al., 2007)

      RelE20 has macrochaeta | ectopic phenotype, enhanceable by scHw-Ua

      (Ayyar et al., 2007)

      RelE20 has mesothoracic tergum phenotype, enhanceable by Tollo1/Tollo[+]

      (Ayyar et al., 2007)

      RelE20 has macrochaeta | ectopic phenotype, enhanceable by Tollo1/Tollo[+]

      (Ayyar et al., 2007)

      RelE20 has mesothoracic tergum phenotype, enhanceable by Dredd[+]/DreddEP1412

      (Ayyar et al., 2007)

      RelE20 has macrochaeta | ectopic phenotype, enhanceable by Dredd[+]/DreddEP1412

      (Ayyar et al., 2007)
      Suppressed by
      Statement
      Reference

      RelE20 has adult fat body | nutrition conditional phenotype, suppressible by foxoW24/foxo[+]

      (Molaei et al., 2019)

      RelE20 has adult fat body | nutrition conditional phenotype, suppressible by Scer\GAL4Cg.PA/foxoKK108485

      (Molaei et al., 2019)

      RelE20 has adult fat body | nutrition conditional phenotype, suppressible by bmmGD5139/Scer\GAL4Cg.PA

      (Molaei et al., 2019)
      Enhancer of
      Statement
      Reference

      RelE20 is an enhancer of wing disc phenotype of dlg1A40.2

      (Parvy et al., 2019)

      RelE20/Rel[+] is an enhancer of eye phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, egrUAS.cMa

      (Tsuda et al., 2010)

      RelE20/Rel[+] is an enhancer of phenotype of Zzzz\repScer\UAS.T:Avic\GFP/Sindbis\repUAS.GFP

      (Avadhanula et al., 2009)

      RelE20 is an enhancer of macrochaeta | ectopic phenotype of scHw-Ua

      (Ayyar et al., 2007)

      RelE20 is an enhancer of mesothoracic tergum phenotype of scHw-Ua

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of mesothoracic tergum phenotype of Tollo1

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of macrochaeta | ectopic phenotype of Tollo1

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of mesothoracic tergum phenotype of DreddEP1412

      (Ayyar et al., 2007)

      RelE20/Rel[+] is an enhancer of macrochaeta | ectopic phenotype of DreddEP1412

      (Ayyar et al., 2007)
      NOT Enhancer of
      Statement
      Reference

      RelE20/Rel[+] is a non-enhancer of flight muscle phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/Rel[+] is a non-enhancer of mitochondrion | adult stage phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/RelE20 is a non-enhancer of flight muscle phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/RelE20 is a non-enhancer of mitochondrion | adult stage phenotype of Pink1B9

      (Lee et al., 2020)
      Suppressor of
      Statement
      Reference

      RelE20 is a suppressor of wing disc phenotype of dlg1A40.2

      (Parvy et al., 2019)

      RelE20/Df(3R)ED5331 is a suppressor of adult brain | progressive phenotype of dnr12-133

      (Cao et al., 2013)

      RelE38/RelE20 is a suppressor of adult brain | progressive phenotype of dnr12-133

      (Cao et al., 2013)

      RelE20 is a suppressor of retina | progressive | conditional phenotype of norpA7

      (Chinchore et al., 2012)

      RelE38/RelE20 is a suppressor of retina | progressive | conditional phenotype of norpA7

      (Chinchore et al., 2012)
      NOT Suppressor of
      Statement
      Reference

      RelE20/Rel[+] is a non-suppressor of flight muscle phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/Rel[+] is a non-suppressor of mitochondrion | adult stage phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/RelE20 is a non-suppressor of flight muscle phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20/RelE20 is a non-suppressor of mitochondrion | adult stage phenotype of Pink1B9

      (Lee et al., 2020)

      RelE20 is a non-suppressor of wing phenotype of PGRP-LF200

      (Maillet et al., 2008)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      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.

      (Lee et al., 2020)

      RelE20 enhances the tumor phenotype and suppress the associated apoptosis (Dcp1 staining) observed in dlg1A40.2 wing discs.

      (Parvy et al., 2019)

      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.

      (Harris et al., 2018)

      When fed Erwinia carotovora, TrpA1ins and RelE20 double mutants display a significantly higher mortality rate than control flies, but not significantly higher than RelE20 mutants.

      RelE20 partially suppresses the increased colony-forming unit gut phenotype of TrpA1ins.

      (Du et al., 2016)

      The increased sensitivity to radiation characteristic for spz4 mutants (whose eclosion rate following irradiation during third larval instar is significantly reduced compared to controls) is not significantly changed by combination with RelE20.

      (Sudmeier et al., 2015)

      Flies heterozygous for both RelE20 and mor1 show a significant decrease in survival following Erwinia carotovora Ecc15 infection.

      Flies heterozygous for both RelE20 and brm2 show a significant decrease in survival following Erwinia carotovora Ecc15 infection.

      (Bonnay et al., 2014)

      RelE20/Df(3R)ED5331 or RelE20/RelE38 significantly suppresses neurodegeneration in dnr12-133/dnr12-133 flies (measured at 29[o]C at 25 days old).

      (Cao et al., 2013)

      The median survival of tefuatm-8 flies is significantly increased if they are also mutant for RelE20.

      The increased apoptotic cell death seen in the brains of heterozygous and homozygous tefuatm-8 adults is significantly suppressed if they are mutant for RelE20.

      (Petersen et al., 2013)

      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.

      (Shravage et al., 2013)

      The increased levels of triacylglycerols and diacylglycerols which are seen in Atf376 larvae are reduced if the larvae are also heterozygous for RelE20. In addition, heterozygosity for RelE20 also reduces the increased levels of free fatty acids seen in Atf376 larvae.

      (Rynes et al., 2012)

      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.

      (Vanha-Aho et al., 2012)

      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.

      (Paredes et al., 2011)

      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.

      (Tsuda et al., 2010)

      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.

      (Costa et al., 2009)

      RelE20 does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF200 mutants.

      (Maillet et al., 2008)

      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.

      (Ayyar et al., 2007)

      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.

      (Kim et al., 2007)

      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.

      (Libert et al., 2006)

      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.

      (Matova and Anderson, 2006)

      RelE20, imd1 double mutant animals are equally susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.

      (Apidianakis et al., 2005)

      The addition of spz4 or Tlrv1/Tlr3 enhances the susceptibility of RelE20 mutants to E.coli and M.luteus infection.

      (De Gregorio et al., 2002)
      Xenogenetic Interactions
      Statement
      Reference

      Heterozygosity for RelE20 in a Scer\GAL4Act5C.PI Zzzz\repScer\UAS.T:Avic\GFP background results in increased Sindbis viral replication.

      (Avadhanula et al., 2009)
      Complementation and Rescue Data
      Fails to complement

      Relunspecified

      (Wu et al., 2001)
      Rescued by

      RelE20 is rescued by RelUAS.Tag:polyHis/Scer\GAL4hs.PB

      (Hedengren et al., 1999)
      Partially rescued by

      RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4Cg.PA

      (Molaei et al., 2019)

      RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4Cg.PA

      (Molaei et al., 2019)

      RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4c564

      (Ryu et al., 2006)

      RelE20 is partially rescued by RelUAS.Tag:polyHis/Scer\GAL4cad-em459

      (Ryu et al., 2006)
      Comments

      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.

      (Molaei et al., 2019)

      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.

      (Ryu et al., 2006)

      RelScer\UAS.T:Zzzz\His6 rescues the immune defects of RelE20 flies when expressed under the control of Scer\GAL4hs.PB.

      (Hedengren et al., 1999)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer

      Induced with: NmdmcE20.

      (Hedengren et al., 1999)
      External Crossreferences and Linkouts ( 1 )
      Crossreferences
      GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
      Synonyms and Secondary IDs (12)
      Reported As
      Symbol Synonym
      Df(3R)E20
      (Lehmann et al., 2002)
      Rel20
      (Libert et al., 2006)
      RelE20
      (Maitra et al., 2021, Lee et al., 2020, Swanson et al., 2020, Aalto et al., 2019, Dudzic et al., 2019, Hanson et al., 2019, Lin et al., 2019, Maitra et al., 2019, Melcarne et al., 2019, Sanchez Bosch et al., 2019, Shukla et al., 2019, Goto et al., 2018, Harris et al., 2018, Li et al., 2018, Lindberg et al., 2018, Nandy et al., 2018, Zhai et al., 2018, Bastos et al., 2017, Dostálová et al., 2017, Khadilkar et al., 2017, Khadilkar et al., 2017, Kurz et al., 2017, Wong et al., 2017, Asaoka et al., 2016, Guillou et al., 2016, Lamiable et al., 2016, Kanoh et al., 2015, Sudmeier et al., 2015, Xiao et al., 2015, Binggeli et al., 2014, Christofi and Apidianakis, 2013, Dantoft et al., 2013, Gendrin et al., 2013, Katzenberger et al., 2013, Petersen et al., 2013, Vanha-Aho et al., 2012, Akhouayri et al., 2011, Paredes et al., 2011, Zaidman-Rémy et al., 2011, Becker et al., 2010, Chen et al., 2010, Buchon et al., 2009, Gendrin et al., 2009, Ha et al., 2009, Ha et al., 2009, Wiklund et al., 2009, Choi et al., 2008, Ratnaparkhi et al., 2008, Ayyar et al., 2007, Kim et al., 2007, Delaney et al., 2006, Kambris et al., 2006, Kambris et al., 2006, Kim et al., 2006, Kim et al., 2006, Matova and Anderson, 2006, Ryu et al., 2006, Scherfer et al., 2006, Zaidman-Remy et al., 2006)
      Rele20
      (Shravage et al., 2013, Clark et al., 2011)
      RelE20
      (Wang et al., 2013)
      RelishE20
      (Iwashita et al., 2020, Dudzic et al., 2019, Valanne et al., 2019, Nonaka et al., 2018, Kenmoku et al., 2017, Tavignot et al., 2017, Bou Sleiman et al., 2015, Bosco-Drayon et al., 2012, Meinander et al., 2012, Tsuzuki et al., 2012, Geuking et al., 2009, Goto et al., 2008, Kleino et al., 2008, Lhocine et al., 2008, Brun et al., 2006, Pili-Floury et al., 2004, Ryu et al., 2004)
      rel20
      (Huang et al., 2017)
      rel20E
      (Brown et al., 2009)
      relE20
      (Iatsenko et al., 2020, Vandehoef et al., 2020, Molaei et al., 2019, Parvy et al., 2019, He et al., 2017, Iatsenko et al., 2016, Cao et al., 2013, Chinchore et al., 2012, Rynes et al., 2012, Wang et al., 2012, Fullaondo et al., 2011, van Uden et al., 2011, Radyuk et al., 2010, Avadhanula et al., 2009, Buchon et al., 2009, Costa et al., 2009, Jones et al., 2008, Wu et al., 2007, Kim et al., 2006, Tang et al., 2006, Apidianakis et al., 2005, Park et al., 2004, Cha et al., 2003, Boutros et al., 2002, Leulier et al., 2000)
      rele20
      (Du et al., 2016, Morris et al., 2016)
      relE20
      (Stefanatos et al., 2013, Wang et al., 2012, Jones et al., 2008)
      relishE20
      (Nagai et al., 2021, Attieh et al., 2020, Iatsenko et al., 2018, Overend et al., 2012, Mueller et al., 2007, Castillejo-Lopez and Häcker, 2005, De Gregorio et al., 2002)
      Name Synonyms
      RelishE20
      (Maillet et al., 2008, Ratnaparkhi et al., 2008, Leulier et al., 2006, Matova and Anderson, 2006)
      relishE20
      (Bonnay et al., 2014, Cao et al., 2013, Narbonne-Reveau et al., 2011, Tsuda et al., 2010, Mulinari et al., 2006)
      Secondary FlyBase IDs
        References (144)