FlyBase Allele Report: Dmel\Dif[1]

General Information

Symbol

Dmel\Dif¹

Species

D. melanogaster

Name

FlyBase ID

FBal0124322

Feature type

allele

Associated gene

Dmel\Dif

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

Nature of the Allele

Allele class

loss of function allele

(Matova and Anderson, 2006)

Mutagen

Progenitor genotype

Cytology

Description

Amino acid replacement: G181D.

(Rutschmann et al., 2000)

Nucleotide substitution: G1104A.

(Rutschmann et al., 2000)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:17,418,565..17,418,565 [-]

Nucleotide change:

G17418565A

Reported nucleotide change:

G1104A

Amino acid change:

G181D | Dif-PA; G181D | Dif-PB; G181D | Dif-PC; G181D | Dif-PD

Reported amino acid change:

G181D

(Rutschmann et al., 2000)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 ( 1 )

Disease

Evidence

References

model of bacterial infectious disease

CEA

(Christofi and Apidianakis, 2013)

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

dorsocentral bristle

(Ayyar et al., 2007)

macrochaeta | ectopic | cold sensitive

(Ayyar et al., 2007)

mesothoracic tergum | ectopic | cold sensitive

(Ayyar et al., 2007)

Detailed Description

Statement

Reference

Dif¹/Df(2L)Exel7068 flies have survival rates similar to wild type in response to Sindbis virus infection.

(Lamiable et al., 2016)

Dif¹/Dif¹ mutants do not exhibit any significant difference in survival rate of flies either untreated or treated with Leishmania amastigotes, as compared to wild type.

(Okuda et al., 2016)

VA1d olfactory receptor neuron axon targeting is normal in mutant flies.

(Ward et al., 2015)

Rel^E20 mutant flies exposed to non-replicating P. aeruginosa bacteria display a mild immunity and slightly extended survival rates compared to non-exposed Dif¹ flies. However, this reaction is not as great as in wild-type flies.

(Christofi and Apidianakis, 2013)

Dif¹/Dif² flies that have been challenged with vesicular stomatitis virus show levels of viral replication that are not significantly different to that seen in wild-type controls.

(Nakamoto et al., 2012)

Mutant flies are highly susceptible to infection with L. monocytogenes (via septic injury) or to infection with B. bassiana.

(Bou Aoun et al., 2011)

Mutant flies show reduced survival compared to wild-type controls after natural infection with B. bassiana.

(Fullaondo et al., 2011)

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.

(Le Bourg, 2011)

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).

(Aymeric et al., 2010)

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.

(Avadhanula et al., 2009)

Short term starvation does not improve the survival of Dif¹ mutant flies following infection with Gram-positive bacteria.

(Brown et al., 2009)

Dif¹ flies show a normal lifespan on dead yeast medium and on live yeast medium. Dif¹ 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)

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.

(Ayyar et al., 2007)

Dif¹/Df(2L)J4 and Dif¹/Dif² larvae do not show R2-R5 photoreceptor axon targeting defects in the developing visual system.

(Minidorff et al., 2007)

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).

(Ryu et al., 2006)

The mean circulating hemocyte number of Dif¹/Df(2L)TW119 mutants is not statistically different from that of controls.

(Chiu 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)

Dif¹ flies show a normal survival rate after natural infection with "Ecc15" (P.carotovorum.carotovorum).

(Ha et al., 2005)

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.

(Zambon et al., 2005)

Dif¹ and Dif¹/Df(2L)J4b mutant flies infected with P.acidolactici, E.faecalis, or S.saprophyticus die more rapidly than wild-type controls.

(Rutschmann et al., 2002)

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 Dif^αTub84B.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.

(Rutschmann et al., 2000)

Mutant flies show lower resistance to B.bassiana (when their cuticles are coated with spores) than wild-type flies, succumbing rapidly to infection.

(Rutschmann et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Dif¹ has increased cell number phenotype, enhanceable by BacA\p35^GMR.PH/Scer\GAL4^He.PZ/dl¹

(Matova and Anderson, 2006)

NOT Enhanced by

Statement

Reference

Dif¹ has abnormal immune response phenotype, non-enhanceable by key¹

(Rutschmann et al., 2002)

Suppressed by

Statement

Reference

Dif¹ has lethal | larval stage phenotype, suppressible by dl^UASp.cMa/dl¹/Scer\GAL4^hs.PB

(Matova and Anderson, 2006)

Dif¹ has lethal | larval stage phenotype, suppressible by Scer\GAL4^e33C/dl^UASp.cMa/dl¹

(Matova and Anderson, 2006)

Dif¹ has lethal | larval stage phenotype, suppressible by dl^UASp.cMa/Scer\GAL4^He.PZ/dl¹

(Matova and Anderson, 2006)

NOT suppressed by

Statement

Reference

Dif¹ has abnormal immune response phenotype, non-suppressible by key¹

(Rutschmann et al., 2002)

NOT Enhancer of

Statement

Reference

Dif¹ is a non-enhancer of short lived phenotype of tefu^atm-8

(Petersen et al., 2013)

Dif¹ is a non-enhancer of increased cell death | adult stage | semidominant phenotype of tefu^atm-8

(Petersen et al., 2013)

Suppressor of

Statement

Reference

Dif¹ is a suppressor | partially of decreased size | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a suppressor | partially of decreased size | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Scer\GAL4^hs.PB, Dif^UAS.cIa, Dif¹ is a suppressor of lethal | larval stage phenotype of dl¹

(Matova and Anderson, 2006)

Df(2L)TW119/Dif¹ is a suppressor | partially of melanotic mass phenotype | larval stage phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005)

NOT Suppressor of

Statement

Reference

Dif¹/Dif¹ is a non-suppressor of abnormal immune response | adult stage phenotype of Diedel¹

(Lamiable et al., 2016)

Dif¹ is a non-suppressor of short lived phenotype of tefu^atm-8

(Petersen et al., 2013)

Dif¹ is a non-suppressor of increased cell death | semidominant | adult stage phenotype of tefu^atm-8

(Petersen et al., 2013)

Dif¹ is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg6¹

(Shravage et al., 2013)

Rel^E20/Dif¹ is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg6¹

(Shravage et al., 2013)

Rel^E20, Df(2L)J4, Dif¹ is a non-suppressor of melanotic mass phenotype | recessive | third instar larval stage phenotype of Atg6¹

(Shravage et al., 2013)

Other

Statement

Reference

Dif¹, key¹ has abnormal immune response | recessive | adult stage phenotype

(Brown et al., 2009)

Dif¹, dl¹ has lethal | larval stage phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has increased cell death phenotype

(Matova and Anderson, 2006)

Dif¹, Rel^E20 has decreased body size phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has abnormal immune response phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has decreased cell number phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has abnormal cell size phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has decreased body size phenotype

(Matova and Anderson, 2006)

Dif¹, Rel^E20 has partially lethal - majority die | larval stage phenotype

(Matova and Anderson, 2006)

Phenotype Manifest In

Enhanced by

Statement

Reference

Dif¹ has hemocyte phenotype, enhanceable by BacA\p35^GMR.PH/Scer\GAL4^He.PZ/dl¹

(Matova and Anderson, 2006)

Suppressed by

Statement

Reference

Dif¹ has hemocyte phenotype, suppressible by Scer\GAL4^e33C/dl^UASp.cMa/dl¹

(Matova and Anderson, 2006)

Dif¹ has hemolymph phenotype, suppressible by Scer\GAL4^e33C/dl^UASp.cMa/dl¹

(Matova and Anderson, 2006)

Dif¹ has hemocyte phenotype, suppressible by dl^UASp.cMa/Scer\GAL4^He.PZ/dl¹

(Matova and Anderson, 2006)

Dif¹ has hemolymph phenotype, suppressible by dl^UASp.cMa/Scer\GAL4^He.PZ/dl¹

(Matova and Anderson, 2006)

Dif¹ has hemocyte phenotype, suppressible by dl^UASp.cMa/Scer\GAL4^srp.Hemo/dl¹

(Matova and Anderson, 2006)

Dif¹ has hemolymph phenotype, suppressible by dl^UASp.cMa/Scer\GAL4^srp.Hemo/dl¹

(Matova and Anderson, 2006)

NOT Enhancer of

Statement

Reference

Rel^E38/Dif¹ is a non-enhancer of medulla phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a non-enhancer of neuropil | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a non-enhancer of adult optic lobe neuron phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a non-enhancer of medulla phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a non-enhancer of neuropil | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a non-enhancer of adult optic lobe neuron phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Suppressor of

Statement

Reference

Dif¹ is a suppressor | partially of adult brain phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a suppressor | partially of adult brain phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a suppressor | partially of lamellocyte | increased number | third instar larval stage phenotype of krz^c01503

(Anjum et al., 2013)

Df(2L)TW119/Dif¹ is a suppressor | partially of hemocyte | increased number phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005)

NOT Suppressor of

Statement

Reference

Dif¹ is a non-suppressor of medulla phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a non-suppressor of neuropil | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a non-suppressor of adult optic lobe neuron phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Rel^E38/Dif¹ is a non-suppressor of medulla phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a non-suppressor of neuropil | adult stage phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Dif¹ is a non-suppressor of adult optic lobe neuron phenotype of Df(3R)BSC519/asp^t25

(Mannino et al., 2023)

Df(2L)TW119/Dif¹ is a non-suppressor of lamellocyte | increased number phenotype of lwr⁵/lwr^4-3

(Chiu et al., 2005)

Other

Statement

Reference

Dif¹, dl¹ has hemocyte phenotype

(Matova and Anderson, 2006)

Dif¹, dl¹ has hemolymph phenotype

(Matova and Anderson, 2006)

Additional Comments

Genetic Interactions

Statement

Reference

Presence of Dif¹/Dif¹ does not suppress the shorter lifespan in Diedel¹/Diedel¹ flies after Sindbis virus infection.

(Lamiable et al., 2016)

Lamellocyte counts are significantly lower in krz^c01503 Dif¹ larvae compared to krz^c01503 larvae.

(Anjum et al., 2013)

Dif¹ fails to suppress the melanotic mass phenotype seen in Atg6¹ mutant third instar larvae.

A Dif¹ Rel^E20 double mutant background fails to suppress the melanotic mass phenotype seen in Atg6¹ mutant third instar larvae.

A Dif¹/Df(2L)J4 Rel^E20 mutant background fails to suppress the melanotic mass phenotype seen in Atg6¹ mutant third instar larvae.

(Shravage et al., 2013)

Short term starvation does not improve the survival of Dif¹-key¹ double mutants following infection with Gram-negative bacteria.

(Brown et al., 2009)

Rel^E20 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 Dif^Scer\UAS.cIa, driven by Scer\GAL4^hs.PB at 25^oC (without heat shock) fully rescues the lethality of Dif¹ dl¹ double mutants.

Ubiquitous expression of dl^Scer\UAS.cMa, driven by Scer\GAL4^hs.PB at 25^oC (without heat shock) fully rescues the lethality of Dif¹ dl¹ double mutants.

Expression of dl^Scer\UAS.cMa in circulating haemocytes, lymph glands, and epidermis, but not in the fat body, under the control of Scer\GAL4^e33C, 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 dl^Scer\UAS.cMa in circulating haemocytes, but not in other immune-responsive tissues, under the control of Scer\GAL4^He.PZ, results in an absence of microbes from the haemolymph, with approximately 45% of dl^Scer\UAS.cMa expressing Dif¹ dl¹ double mutants surviving till adulthood.

Expression of dl^Scer\UAS.cMa in circulating haemocytes and lymph gland cells, under the control of Scer\GAL4^srp.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.

(Matova and Anderson, 2006)

The melanotic tumour penetrance and circulating hemocyte levels are partially reduced in lwr^4-3 Df(2L)TW119/lwr⁵ Dif¹ double mutants, compared to lwr^4-3/lwr⁵ single mutants. However, the amount of lamellocytes is not reduced.

(Chiu et al., 2005)

Dif¹ key¹ double mutants die at the same rate as Dif¹ single mutants when infected with either P.acidolactici, E.faecalis, or S.saprophyticus.

(Rutschmann et al., 2002)

Dif¹ key¹ double mutants die at the same rate as Dif¹ mutants when their cuticles are coated with spores of B.bassiana.

(Rutschmann et al., 2000)

Xenogenetic Interactions

Statement

Reference

Expression of BacA\p35^GMR.PH in the haemocytes, under the control of Scer\GAL4^He.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.

(Matova and Anderson, 2006)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

36559

P{Dipt2.2-lacZ}1, P{Drs-GFP.JM804}1, y¹ w^*; Dif¹ cn¹ bw¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

dif1

(Nunes et al., 2021)

dif¹

(Mannino et al., 2023, Bahuguna et al., 2022)

Name Synonyms

Secondary FlyBase IDs

References (48)

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