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General Information
Symbol
Dmel\imd1
Species
D. melanogaster
Name
FlyBase ID
FBal0045906
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
imd
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    point mutation
    Nucleotide change:

    C18411319T

    Amino acid change:

    A31V | imd-PA; A31V | imd-PB

    Reported amino acid change:

    A31V

    Comment:

    Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Amino acid replacement: A31V.

    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 ( 0 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference

    imd1/imd1 flies have survival rates similar to wild type in response to Sindbis virus infection.

    imd1/imd1 mutants exhibit a significant decrease in survival in response to P. rettgeri infection, as compared to wild type.

    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.

    Infection with the S. aureus 'ItaS' mutant causes earlier death than infection with its parent RN4220 strain in imd1 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.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhancer of
    Statement
    Reference

    imd1 is an enhancer of tumorigenic | larval stage phenotype of dlg1A40.2

    NOT Enhancer of
    Statement
    Reference

    imd1 is a non-enhancer of neuroanatomy defective | adult stage | progressive | conditional phenotype of norpA7

    Suppressor of
    Statement
    Reference
    NOT Suppressor of
    Statement
    Reference

    imd1 is a non-suppressor of neuroanatomy defective | adult stage | progressive | conditional phenotype of norpA7

    Other
    Phenotype Manifest In
    Enhancer of
    Statement
    Reference

    imd1 is an enhancer of wing disc phenotype of dlg1A40.2

    NOT Enhancer of
    Statement
    Reference

    imd1 is a non-enhancer of retina | progressive | conditional phenotype of norpA7

    Suppressor of
    Statement
    Reference

    imd1 is a suppressor of wing disc phenotype of dlg1A40.2

    imd1 is a suppressor of wing phenotype of PGRP-LF200

    NOT Suppressor of
    Statement
    Reference

    imd1 is a non-suppressor of retina | progressive | conditional phenotype of norpA7

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    imd1 enhances the tumor phenotype and suppress the associated apoptosis (Dcp1 staining) observed in dlg1A40.2 wing discs

    Presence of imd1/imd1 partially suppresses the shorter lifespan in Diedel1/Diedel1 flies after Sindbis virus infection.

    imd1 suppresses the notching phenotypes and low adult viability seen in homozygous PGRP-LF200 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.

    domk08108 imd1 double mutant larvae show a dramatically compromised survival after injury (whether it is a clean injury or an injury combined with infection).

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    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.

    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer
    Comments
    Comments

    Bacterially challenged larvae exhibit severely impaired expression of the antibacterial peptide genes and survival is decreased.

    Homozygotes show attenuated induction of immunity genes such as CecA1 and Dpt.

    Synthesis of antibacterial peptides is impaired.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (4)
    References (51)