Amino acid replacement: G181D.
Nucleotide substitution: G1104A.
G17418565A
G1104A
G181D | Dif-PA; G181D | Dif-PB; G181D | Dif-PC; G181D | Dif-PD
G181D
Dif1/Df(2L)Exel7068 flies have survival rates similar to wild type in response to Sindbis virus infection.
VA1d olfactory receptor neuron axon targeting is normal in mutant flies.
Mutant flies are highly susceptible to infection with L. monocytogenes (via septic injury) or to infection with B. bassiana.
Mutant flies show reduced survival compared to wild-type controls after natural infection with B. bassiana.
Dif1 flies infected at 2-4 days of age exhibit a shorter survival time than control flies, regardless of sex. Approximately 15% of Dif1 flies die in the first two days of life, regardless of infection. Control flies live long than Dif1 flies, with fungal infection slightly decreasing longevity in both sets of flies, regardless of sex.
In controlled conditions, where flies are virgin, and larvae aren't crowded, Dif1 flies outlive control flies, and females outlive males.
Dif1 flies do not exhibit a difference to controlled flies in terms of resistance to heat.
Dif1 mutant flies survive for a shorter time after fungal infection, compared to controls, with males tending to survive slightly longer than females, while no sex difference is seen in controls.
Mutant flies that are infected with E. coli one day prior to infection with either X. nematophila or P. luminescens show the same phenotype as wild-type flies (increased survival after infection with either X. nematophila or P. luminescens due to partial protection by the prior infection with E. coli).
Dif1 mutant flies show similar levels of viral replication and viral titers 5 days after intrathoracic infection with 200 pfu of Sindbis virus as controls.
Short term starvation does not improve the survival of Dif1 mutant flies following infection with Gram-positive bacteria.
Homozygous flies show ectopic macrochaetae in 29% 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 8% of heminota at 18[o]C.
Dif1 flies show similar mortality levels to wild-type flies in response to feeding with both the ROS-resistant KNU53775 yeast strain and a standard yeast strain (W303).
The mean circulating hemocyte number of Dif1/Df(2L)TW119 mutants is not statistically different from that of controls.
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.
Dif1 flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).
Dif1 mutant flies exhibit increased susceptibility to DXV virus infection compared to wild-type. Dif1 flies succomb to anoxia induced death approximately 48 hours earlier than wild-type. Viral titer levels are also found to be approximately 40-times higher than observed in wild-type at 3 days post-infection.
Flies hemizygous for Dif1/Df(2L)J4b exhibit an extreme reduction in the inducibility of Drs 48hrs after immune challenge. In contrast, Dif1/Df(2L)J4b flies carrying DifαTub84B.PM express Drs at almost wild-type levels under similar conditions.
Dif1 mutant flies are significantly more sensitive to fungal infection than wild-type flies. Two and a half days after infection with the entomopathogenic fungus B. bassiana, most Dif1 mutants have died, whereas ~90% of the wild-type flies are still alive. The survival curves are similar for homozygous and hemizygous Dif1/Df(2L)TW119 flies.
Dif1 mutants display a resistance to bacterial infections (whether gram-positive, gram-negative, or mixtures), similar to that of wild-type flies.
Mutant flies show lower resistance to B.bassiana (when their cuticles are coated with spores) than wild-type flies, succumbing rapidly to infection.
Dif1 has increased cell number phenotype, enhanceable by BacA\p35GMR.PH/Scer\GAL4He.PZ/dl1
Dif1 has abnormal immune response phenotype, non-enhanceable by key1
Dif1 has lethal | larval stage phenotype, suppressible by dlUASp.cMa/dl1/Scer\GAL4hs.PB
Dif1 has lethal | larval stage phenotype, suppressible by Scer\GAL4e33C/dlUASp.cMa/dl1
Dif1 has lethal | larval stage phenotype, suppressible by dlUASp.cMa/Scer\GAL4He.PZ/dl1
Dif1 has abnormal immune response phenotype, non-suppressible by key1
Dif1 is a non-enhancer of short lived phenotype of tefuatm-8
Dif1 is a non-enhancer of increased cell death | adult stage | semidominant phenotype of tefuatm-8
Dif1 is a suppressor | partially of decreased size | adult stage phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a suppressor | partially of decreased size | adult stage phenotype of Df(3R)BSC519/aspt25
Scer\GAL4hs.PB, DifUAS.cIa, Dif1 is a suppressor of lethal | larval stage phenotype of dl1
Df(2L)TW119/Dif1 is a suppressor | partially of melanotic mass phenotype | larval stage phenotype of lwr5/lwr4-3
Dif1/Dif1 is a non-suppressor of abnormal immune response | adult stage phenotype of Diedel1
Dif1 is a non-suppressor of short lived phenotype of tefuatm-8
Dif1 is a non-suppressor of increased cell death | semidominant | adult stage phenotype of tefuatm-8
Dif1 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
Dif1, key1 has abnormal immune response | recessive | adult stage phenotype
Dif1, dl1 has lethal | larval stage phenotype
Dif1, dl1 has increased cell death phenotype
Dif1, RelE20 has decreased body size phenotype
Dif1, dl1 has abnormal immune response phenotype
Dif1, dl1 has decreased cell number phenotype
Dif1, dl1 has abnormal cell size phenotype
Dif1, dl1 has decreased body size phenotype
Dif1, RelE20 has partially lethal - majority die | larval stage phenotype
Dif1 has hemocyte phenotype, enhanceable by BacA\p35GMR.PH/Scer\GAL4He.PZ/dl1
Dif1 has hemocyte phenotype, suppressible by Scer\GAL4e33C/dlUASp.cMa/dl1
Dif1 has hemolymph phenotype, suppressible by Scer\GAL4e33C/dlUASp.cMa/dl1
Dif1 has hemocyte phenotype, suppressible by dlUASp.cMa/Scer\GAL4He.PZ/dl1
Dif1 has hemolymph phenotype, suppressible by dlUASp.cMa/Scer\GAL4He.PZ/dl1
Dif1 has hemocyte phenotype, suppressible by dlUASp.cMa/Scer\GAL4srp.Hemo/dl1
Dif1 has hemolymph phenotype, suppressible by dlUASp.cMa/Scer\GAL4srp.Hemo/dl1
RelE38/Dif1 is a non-enhancer of medulla phenotype of Df(3R)BSC519/aspt25
Dif1 is a non-enhancer of neuropil | adult stage phenotype of Df(3R)BSC519/aspt25
Dif1 is a non-enhancer of adult optic lobe neuron phenotype of Df(3R)BSC519/aspt25
Dif1 is a non-enhancer of medulla phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a non-enhancer of neuropil | adult stage phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a non-enhancer of adult optic lobe neuron phenotype of Df(3R)BSC519/aspt25
Dif1 is a suppressor | partially of adult brain phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a suppressor | partially of adult brain phenotype of Df(3R)BSC519/aspt25
Dif1 is a suppressor | partially of lamellocyte | increased number | third instar larval stage phenotype of krzc01503
Df(2L)TW119/Dif1 is a suppressor | partially of hemocyte | increased number phenotype of lwr5/lwr4-3
Dif1 is a non-suppressor of medulla phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a non-suppressor of neuropil | adult stage phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a non-suppressor of adult optic lobe neuron phenotype of Df(3R)BSC519/aspt25
RelE38/Dif1 is a non-suppressor of medulla phenotype of Df(3R)BSC519/aspt25
Dif1 is a non-suppressor of neuropil | adult stage phenotype of Df(3R)BSC519/aspt25
Dif1 is a non-suppressor of adult optic lobe neuron phenotype of Df(3R)BSC519/aspt25
Df(2L)TW119/Dif1 is a non-suppressor of lamellocyte | increased number phenotype of lwr5/lwr4-3
Dif1 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.
RelE20 Dif1 double mutant larvae are smaller than wild-type, and about half of the double homozygotes die before reaching adult stages.
Dif1 dl1 double mutants are small and sluggish and only 3.4% survive to adult. Unchallenged Dif1 dl1 double mutant larvae contain many bacteria and yeast in their haemolymph (as many as 105 microbes per animal), while no microbes are observed in wild-type haemolymph. In microbe-free conditions, in the presence of antibiotics, approximately 33% of Dif1 dl1 double mutants survive to adult stages, thats a 10-fold increase compared to normal conditions. Dif1 dl1 double mutants are able to mount a humoral immune response, but this does not prevent constitutive infection of these animals.
Dif1 dl1/+ + double heterozygotes exhibit approximately 5000 blood cells per υl of haemolymph, the same as in wild-type flies. In contrast, Dif1 dl1 double homozygotes exhibit a greatly reduced number of haemocytes, approximately 500 per υl - 10-fold fewer than in wild-type. Approximately 15% of Dif1 dl1 haemocytes undergo apoptosis, compared with only 2.3% in wild-type.
The few blood cells present in Dif1 dl1 mutants exhibit an abnormal morphology. In contrast to wild-type haemocytes, Dif1 dl1 blood cells are enlarged, containing intact intracellular bacteria that are not localised to vacuoles and have not been digested. When Dif1 dl1 larvae are grown on minimal medium in the presence of antibiotics, the number of haemocytes increases 3-fold, to approximately 1400 cells per υl, and the haemocytes are of normal morphology.
Ubiquitous expression of DifScer\UAS.cIa, driven by Scer\GAL4hs.PB at 25oC (without heat shock) fully rescues the lethality of Dif1 dl1 double mutants.
Ubiquitous expression of dlScer\UAS.cMa, driven by Scer\GAL4hs.PB at 25oC (without heat shock) fully rescues the lethality of Dif1 dl1 double mutants.
Expression of dlScer\UAS.cMa in circulating haemocytes, lymph glands, and epidermis, but not in the fat body, under the control of Scer\GAL4e33C, restores normal haemocyte numbers in Dif1 dl1 double mutants. The rescued blood cells are indistinguishable in morphology from wild-type uninfected haemocytes. In addition, the rescued animals have do not have any microbes in their haemolymph and 66% survive to adult stages.
Expression of dlScer\UAS.cMa in circulating haemocytes, but not in other immune-responsive tissues, under the control of Scer\GAL4He.PZ, results in an absence of microbes from the haemolymph, with approximately 45% of dlScer\UAS.cMa expressing Dif1 dl1 double mutants surviving till adulthood.
Expression of dlScer\UAS.cMa in circulating haemocytes and lymph gland cells, under the control of Scer\GAL4srp.Hemo, increases blood cell number to approximately 90% of wild-type in Dif1 dl1 double mutants and enables approximately 50% survival till adulthood. The majority of these larvae have no microbes in their haemolymph.
Dif1 key1 double mutants die at the same rate as Dif1 mutants when their cuticles are coated with spores of B.bassiana.
Expression of BacA\p35GMR.PH in the haemocytes, under the control of Scer\GAL4He.PZ in Dif1 dl1 animals results in the number of blood cells per υl of haemolymph increasing 4-fold, to approximately 2200 cells per υl, whereas the blood cell number remains constant in Dif1 dl1 heterozygotes.