Amino acid replacement: A31V.
C18411319T
A31V | imd-PA; A31V | imd-PB
A31V
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
imd1 adults show increased susceptibility (i.e. mortality) to Ecc15 bacterial infection.
imd1 homozygotes show defective immune response to Enterobacter cloacae, as flies show increased mortality.
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.
Mutant animals, like wild-type, are significantly less susceptible to P.aeruginosa PA14 virulent strain after infection with the CF5 avirulent strain.
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.
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.
imd1 has abnormal immune response | adult stage phenotype, non-suppressible by DyroΔ6/DyroΔ6
imd1 has short lived | adult stage | conditional phenotype, non-suppressible by DyroΔ6/DyroΔ6
imd1 is an enhancer of neoplasia | larval stage phenotype of dlg1A40.2
imd1 is a non-enhancer of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpAEE5
imd1 is a suppressor of increased cell death | larval stage phenotype of dlg1A40.2
imd1/imd1 is a suppressor | partially of abnormal immune response | adult stage phenotype of Diedel1
imd1 is a suppressor of partially lethal - majority die phenotype of PGRP-LF200
imd1 is a suppressor of visible | adult stage phenotype of PGRP-LF200
imd1 is a non-suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpAEE5
DyroΔ6, imd1 has short lived phenotype
RelE20, imd1 has abnormal immune response phenotype
imd1, spz4 has abnormal immune response phenotype
imd1 is a non-enhancer of retina | progressive | conditional phenotype of norpAEE5
imd1 is a suppressor of wing phenotype of PGRP-LF200
imd1 is a non-suppressor of retina | progressive | conditional phenotype of norpAEE5
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.
imd1 is rescued by imdUAS.cGa/Scer\GAL4hs.PB
Arose on: Bc1.
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.