A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\imd1

General Information
SymbolDmel\imd1SpeciesD. melanogaster
NameFlyBase IDFBal0045906
Feature typealleleAssociated geneDmel\imd
Also Known Asimd
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0045906
Allele classhypomorphic allele - genetic evidence
Mutagen
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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
References
point mutation
comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
evidence=experimental
pr_change=A31V|imd-PA
reported_pr_change=A31V
na_change=C14298824T
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Amino acid replacement: A31V.
Cytology
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Statement
Reference
Infection with the S. aureus 'ItaS' mutant causes earlier death than infection with its parent RN4220 strain in imd[1] flies, similar to the findings with wild type flies.
Mutant flies show reduced survival compared to wild-type flies after exposure to the Gram-negative bacteria E.cloacae.
imd1 mutant females are more susceptible post-bacterial-infection than males. spz4 mutant males can withstand B.bassiana fungal infection to a greater level than imd1 mutant females.
Mutant animals, like wild-type, are significantly less susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
imd1; spz4 double homozygotes show 90% lethality in response to infection with M.luteus, compared to no significant lethality in infected wild-type animals. imd1; spz4 double homozygotes infected with B.subtilis or S.aureus die significantly more rapidly than infected wild-type animals.
The survival rate of imd1 homozygous adults infected by pricking with a mixture of E.coli and M.luteus is significantly lower than that for wild-type but significantly higher than that for imd1/Df(2R)2.1 flies. The proportion of imd1 homozygous pupae (24 hours APF) surviving to adulthood after UV irradiation (50,000 μJ/cm2) is significantly higher than for wild-type.
After infection with P.carotovorum, the bacteria persist longer in imd1 mutants than in wild-type.
4 days after infection with S. epidermis only 66% of mutant flies survive, compared to over 80% in wild-type. 4 days after infection with M. roseus, 2% of mutant flies survive as compared to 46% in wild-type.
Mutant adults are 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.
There is not a significant difference in the survival rate between larvae pricked with a sterile needle or a needle coated with Gram-positive or Gram-negative bacteria.
Homozygotes are highly sensitive to infection, with approximately 80% dying within 5 days after infection with E.cloacae. Severe impairment of the normal immune response.
Inducibility of all antimicrobial genes by bacterial challenge in imd1/imd1; Tlr3/Tlrv1 double mutants is severely reduced. Septic injury (pricking with a needle under nonsterile conditions) does not noticeably affect imd1 homozygote survival, infection with A.fumigatus results 93% survival 3 days postinfection and 3 days postinfection with E. coli there are a few survivors (8% survival). 40% homozygous double mutant flies survive after septic injury but only a few individuals survive 3 days postinfection with E.coli.
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Statement
Reference
imd1 is a suppressor of visible | adult stage phenotype of PGRP-LF200
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Statement
Reference
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hideSuppressor of
Statement
Reference
imd1 is a suppressor of wing phenotype of PGRP-LF200
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Statement
Reference
imd[1] suppresses the notching phenotypes and low adult viability seen in homozygous PGRP-LF[200] mutants.
RelE20, imd1 double mutant animals are equally susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
Lethality in imd1; spz4 double homozygotes in response to M.luteus infection is suppressed by DptScer\UAS.cTa/DptScer\UAS.cTa; Scer\GAL4da.G32, and partially suppressed by DroScer\UAS.cTa/DroScer\UAS.cTa; Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to B.subtilis infection is suppressed by DefScer\UAS.cTa/DefScer\UAS.cTa; Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to S.aureus infection is significantly delayed by DefScer\UAS.cTa/DefScer\UAS.cTa; Scer\GAL4da.G32. The addition of a third copy of DefScer\UAS.cTa further delays the death of these flies. This protective effect is not enhanced by the presence of DptScer\UAS.cTa, DroScer\UAS.cTa, CecA1Scer\UAS.cTa, AttAScer\UAS.cTa, or DrsScer\UAS.cTa. Lethality in imd1; spz4 double homozygotes in response to E.coli infection is significantly delayed by AttAScer\UAS.cTa/AttAScer\UAS.cTa; Scer\GAL4da.G32, or AttAScer\UAS.cTa/DroScer\UAS.cTa; Scer\GAL4da.G32, or AttAScer\UAS.cTa/DptScer\UAS.cTa; Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to E.carotorva infection is significantly delayed by AttAScer\UAS.cTa/AttAScer\UAS.cTa; Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to A.tumefaciens infection is significantly delayed by DroScer\UAS.cTa/DroScer\UAS.cTa; Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to P.aeruginosa infection is unaffected by expression of DptScer\UAS.cTa, DroScer\UAS.cTa, CecA1Scer\UAS.cTa, AttAScer\UAS.cTa, DrsScer\UAS.cTa, or DefScer\UAS.cTa with Scer\GAL4da.G32. Lethality in imd1; spz4 double homozygotes in response to infection with N.crassa or F.oxysporum is restored to wild-type levels by DrsScer\UAS.cTa/DrsScer\UAS.cTa; Scer\GAL4da.G32. This effect requires at least two copies of DrsScer\UAS.cTa. Lethality in imd1; spz4 double homozygotes in response to A.fumigatus infection is significantly delayed by DrsScer\UAS.cTa/DrsScer\UAS.cTa; Scer\GAL4da.G32. This effect requires at least two copies of DrsScer\UAS.cTa. Lethality in imd1; spz4 double homozygotes in response to cuticular deposition of B.bassiana spores is unaffected by expression of DptScer\UAS.cTa, DroScer\UAS.cTa, CecA1Scer\UAS.cTa, AttAScer\UAS.cTa, DrsScer\UAS.cTa, or DefScer\UAS.cTa with Scer\GAL4da.G32. N.crassa does not sporulate on the corpses of imd1 DrsScer\UAS.cTa/imd1; spz4 DrsScer\UAS.cTa/spz4 Scer\GAL4da.G32 flies.
imd1; spz4 adults are highly susceptible to infection by E.coli or M.luteus (survival rate is reduced after pricking with an infected needle compared to survival rate of control flies). The adults are highly sensitive to natural infection by B.bassiana or injection of A.fumigatus spores.
dom[k08108] imd[1] double mutant larvae show a dramatically compromised survival after injury (whether it is a clean injury or an injury combined with infection).
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Statement
Reference
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Rescued by
Comments
The presence of imd+t5.1 rescues the survival rate of imd1 homozygotes infected with a mixture of E.coli and M.luteus to wild-type levels.
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Homozygotes show attenuated induction of immunity genes such as CecA1 and Dpt.
Synthesis of antibacterial peptides is impaired.
Bacterially challenged larvae exhibit severely impaired expression of the antibacterial peptide genes and survival is decreased.
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hide Recent research papers ( 4 )
Longworth et al., 2012, PLoS Genet. 8(4): e1002618
A Shared Role for RBF1 and dCAP-D3 in the Regulation of Transcription with Consequences for Innate Immunity. [FBrf0218058]
Neyen et al., 2012, J. Immunol. 189(4): 1886--1897
Tissue- and Ligand-Specific Sensing of Gram-Negative Infection in Drosophila by PGRP-LC Isoforms and PGRP-LE. [FBrf0219094]
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]
Akhouayri et al., 2011, PLoS Pathog. 7(10): e1002319
Toll-8/tollo negatively regulates antimicrobial response in the Drosophila respiratory epithelium. [FBrf0216452]