FlyBase Allele Report: Dmel\G9a[DD2]

General Information

Symbol

Dmel\G9a^DD2

Species

D. melanogaster

Name

FlyBase ID

FBal0260882

Feature type

allele

Associated gene

Dmel\G9a

Associated Insertion(s)

Carried in Construct

Also Known As

EHMT^DD2

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - molecular evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

hypomorphic allele - molecular evidence

(Kramer et al., 2011)

Mutagen

Delta2-3 transposase

(Kramer et al., 2011)

Progenitor genotype

P{SUPor-P}G9a^KG01242

(Kramer et al., 2011)

Cytology

Description

Imperfect excision of P{SUPor-P}G9a^KG01242, resulting in loss of 1473 bp of DNA downstream of the insertion site which includes the translational start site.

(Kramer et al., 2011)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

X:246,142..247,614 [+]

Comment:

1473 bp deletion resulting from the imprecise excsion of P{SUPor-P}G9a^KG01242 removes the G9a translation start site.

(Kramer et al., 2011)

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 viral infectious disease

CEA

(Merkling et al., 2015)

model of Kleefstra syndrome 1

CEA

(Kramer et al., 2011)

CEA with G9a^DD1

(Kramer et al., 2011)

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

larval ventral cluster group multidendritic neuron

(Kramer et al., 2011)

multidendritic dendrite | third instar larval stage

(Kramer et al., 2011)

Detailed Description

Statement

Reference

G9a^DD2 homozygous adults exhibit increased mortality upon systematic infection with a range of doses of Drosophila C Virus (DCV) compared to controls. When challenged with the highest dose (10[9]) mortality is similar between mutants and controls. The viral load increases in a dose-dependent manner in both mutants and controls. Female flies achieve higher viral loads measured 5 days post-DCV-infection compared to males and the sensitivity to infection difference between mutants and controls is much higher in females than males. According to nonlinear 4-parameter logistic model, mutants are more sensitive to increasing viral doses while there is no difference between mutants and controls in the severity of infection.

(Gupta and Vale, 2017)

The average life span of G9a^DD2 is slightly longer than that of wild-type controls.

G9a^DD2 mutant flies show increased sensitivity to infection by Drosophila C virus (DCV), Cricket paralysis virus (CrPV), Flock House Virus (FHV), Drosophila X Virus (DXV) relative to wild-type. The mutant flies show reduced survival after RNA virus infection compared with wild-type. Survival rates of G9a^DD2 mutants after infection with the DNA virus Invertebrate iridescent virus 6 (IIV-6) are similar to wild-type. No significant difference is detected in DCV viral titers between mutant and wild-type flies, indicating that G9a^DD2 mutants show reduced tolerance to RNA virus infection.

(Merkling et al., 2015)

General nervous system development and neuronal function is not affected in mutant flies.

Dendrite development in multidendrite (md) neurons is altered in mutant flies. While the basic organization of dendritic arbours in type 4 md neurons is maintained, there is a reduction of higher order branching resulting in dendritic fields of appreciably reduced complexity. The total number of dendrite ends is significantly reduced.

The total path length covered by foraging mutant larvae is not different from controls. However, mutant larvae often stop, retract and turn, causing increased branching in their crawling paths.

Adult phototaxis and geotaxis behaviours are normal in mutants.

Hemizygous males and G9a^DD1/G9a^DD2 females both display a drastically slower response decrement during habituation to a "light-off jump reflex" compared to controls.

Short-term courtship memory of G9a^DD2 males is reduced compared to controls.

(Kramer et al., 2011)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

G9a^DD2 has abnormal immune response phenotype, non-enhanceable by dome^ΔCYT.UAS/Scer\GAL4^Act.PU

(Merkling et al., 2015)

G9a^DD2 has short lived | conditional phenotype, non-enhanceable by dome^ΔCYT.UAS/Scer\GAL4^Act.PU

(Merkling et al., 2015)

G9a^DD2 has abnormal immune response phenotype, non-enhanceable by Scer\GAL4^Act.PU/Socs36E^UASp.cCa

(Merkling et al., 2015)

G9a^DD2 has short lived | conditional phenotype, non-enhanceable by Scer\GAL4^Act.PU/Socs36E^UASp.cCa

(Merkling et al., 2015)

NOT suppressed by

Statement

Reference

G9a^DD2 has abnormal immune response phenotype, non-suppressible by dome^ΔCYT.UAS/Scer\GAL4^Act.PU

(Merkling et al., 2015)

G9a^DD2 has short lived | conditional phenotype, non-suppressible by dome^ΔCYT.UAS/Scer\GAL4^Act.PU

(Merkling et al., 2015)

G9a^DD2 has abnormal immune response phenotype, non-suppressible by Scer\GAL4^Act.PU/Socs36E^UASp.cCa

(Merkling et al., 2015)

G9a^DD2 has short lived | conditional phenotype, non-suppressible by Scer\GAL4^Act.PU/Socs36E^UASp.cCa

(Merkling et al., 2015)

NOT Suppressor of

Statement

Reference

G9a^DD2 is a non-suppressor of increased cell death phenotype of Diap1^RNAi.UAS, Scer\GAL4^GMR.PF

(Merkling et al., 2015)

Phenotype Manifest In

NOT Suppressor of

Statement

Reference

G9a^DD2 is a non-suppressor of eye phenotype of Diap1^RNAi.UAS, Scer\GAL4^GMR.PF

(Merkling et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

G9a^DD2 is rescued by G9a^UAS.cKa

(Merkling et al., 2015)

G9a^DD2 is rescued by G9a^UAS.cKa/Scer\GAL4^elav.PLu

(Kramer et al., 2011)

G9a^DD2 is rescued by G9a^UAS.cKa/Scer\GAL4^7B

(Kramer et al., 2011)

Partially rescued by

G9a^DD2 is partially rescued by G9a^UAS.cKa/Scer\GAL4⁴⁷⁷

(Kramer et al., 2011)

Not rescued by

G9a^DD2 is not rescued by G9a^UAS.cKa/Scer\GAL4^repo

(Merkling et al., 2015)

G9a^DD2 is not rescued by Scer\GAL4^Hml.PG/G9a^UAS.cKa

(Merkling et al., 2015)

G9a^DD2 is not rescued by G9a^UAS.cKa/Scer\GAL4⁴⁷⁷

(Kramer et al., 2011)

Comments

The early lethality of DCV infected G9a^DD2 mutants is rescued to control levels by fat body-specific expression of G9a^Scer\UAS.cKa under the control of Scer\GAL4^c564.

Expression of G9a^Scer\UAS.cKa under the control of either Scer\GAL4^Hml.PG or Scer\GAL4^repo fails to rescue the hypersensitivity of G9a^DD2 mutant flies to DCV infection.

(Merkling et al., 2015)

Expression of G9a^Scer\UAS.cKa using Scer\GAL4⁴⁷⁷ in a G9a^DD2 background rescues dendrite branching towards wild type levels.

Expression of G9a^Scer\UAS.cKa using Scer\GAL4⁴⁷⁷ in a G9a^DD2 background fails to restore normal larval locomotor behaviour.

Expression of G9a^Scer\UAS.cKa using Scer\GAL4^elav.PLu or Scer\GAL4^7B restores the short-term courtship memory defect of G9a^DD2 males.

(Kramer et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

EHMT^DD2

(Lo and Chen, 2019, Kramer et al., 2011)

G9a^DD2

(Gupta and Vale, 2017, Merkling et al., 2015)

Name Synonyms

Secondary FlyBase IDs

References (4)

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