FlyBase Allele Report: Dmel\HtrA2[Δ1]

General Information

Symbol

Dmel\HtrA2^Δ1

Species

D. melanogaster

Name

FlyBase ID

FBal0230523

Feature type

allele

Associated gene

Dmel\HtrA2

Associated Insertion(s)

Carried in Construct

Also Known As

omi^Δ1

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - molecular evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Tain et al., 2009)

Mutagen

P-element activity

(Tain et al., 2009)

Progenitor genotype

P{EP}mRpL11^G4907

(Tain et al., 2009)

Caused by aberration

Df(3R)HtrA2^Δ1

Cytology

Description

Imprecise excision of the progenitor insertion, resulting in a 1037bp deletion that extends from the site of the original insertion to exon 1 of HtrA2, leaving 8bp of exon 1. The promoter region and transcription start site of the mRpL11 gene are also missing.

(Tain et al., 2009)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3R:14,510,857..14,511,893 [-]

Comment:

1037 bp deletion resulting from the imprecise excision of P{EP}mRpL11^G4907, which extends from the site of the insertion into exon 1 of HtrA2.

(Tain et al., 2009)

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 Parkinson's disease

CEA

(Tain et al., 2009)

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

abnormal locomotor behavior

(Tain et al., 2009)

chemical sensitive

(Tain et al., 2009)

female fertile

(Yacobi-Sharon et al., 2013, Tain et al., 2009)

flightless

(Tain et al., 2009)

male sterile

(Yacobi-Sharon et al., 2013, Tain et al., 2009)

short lived

(Tain et al., 2009)

viable

(Yacobi-Sharon et al., 2013)

Phenotype Manifest In

male germline cell

(Yacobi-Sharon et al., 2013)

mitochondrion & indirect flight muscle

(Tain et al., 2009)

spermatogonial cyst

(Yacobi-Sharon et al., 2013)

spermatozoon

(Tain et al., 2009)

Detailed Description

Statement

Reference

Homozygous HtrA2^Δ1 mutant flies display a 50%-60% reduction in spermatogonial cyst death compared to wild type controls.

(Yacobi-Sharon et al., 2013)

The development of HtrA2^Δ1 animals (Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0) is completely normal, in particular, showing normal eye morphology.

HtrA2^Δ1 mutant wing discs (from Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0) show identical apoptosis induction in response to treatment with γ-rays, staurosporine or ultraviolet light compared to control discs, and also show identical levels of apoptosis to control discs in the absence of any treatment.

Overall structure of the indirect flight muscles (IFMs) is maintained in 30 day old HtrA2^Δ1 animals (Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0). However, ultrastructural defects are seen in the IFMs in these animals; there are increased numbers of defective mitochondria, displaying reduced electron density and open cristae, compared to controls. There is no systematic mitochondrial deficiency in the mutant animals.

HtrA2^Δ1 animals (Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0) show normal flight and climbing ability at 5 days of age. However, 30 day old mutant flies have significantly reduced flight and climbing ability compared with controls. The number of dopaminergic neurons is normal in the 30 day old mutant flies.

HtrA2^Δ1 males (Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0) show 4% fertility compared to controls. Mature individualised sperm are formed properly in the mutant testes, but they are completely immotile.

HtrA2^Δ1 animals (Df(3R)HtrA2^Δ1 homozygotes in which the loss of mRpL11 function has been rescued by two copies of mRpL11^+t2.0) have a reduced lifespan compared to controls. They also show increased sensitivity to paraquat and rotenone compared to controls.

(Tain et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

HtrA2^Δ1 is an enhancer of abnormal locomotor behavior phenotype of park²⁵

(Tain et al., 2009)

NOT Enhancer of

Statement

Reference

HtrA2^Δ1 is a non-enhancer of abnormal locomotor behavior phenotype of Pink1^B9

(Tain et al., 2009)

Suppressor of

Statement

Reference

HtrA2^Δ1 is a suppressor of visible | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park²⁵

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor | partially of visible | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor | partially of visible phenotype of Scer\GAL4^GMR.PF, rho-7^UAS.cWa

(Whitworth et al., 2008)

NOT Suppressor of

Statement

Reference

HtrA2^Δ1 is a non-suppressor of abnormal locomotor behavior phenotype of Pink1^B9

(Tain et al., 2009)

HtrA2^Δ1 is a non-suppressor of visible | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park^UAS.cGa

(Whitworth et al., 2008)

HtrA2^Δ1 is a non-suppressor of visible phenotype of Scer\GAL4^GMR.PF, park^UAS.cGa, rho-7^UAS.cWa

(Whitworth et al., 2008)

Phenotype Manifest In

Suppressor of

Statement

Reference

HtrA2^Δ1 is a suppressor | partially of ommatidium | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor | partially of eye phenotype of Scer\GAL4^GMR.PF, rho-7^UAS.cWa

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor | partially of interommatidial bristle phenotype of Scer\GAL4^GMR.PF, rho-7^UAS.cWa

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor of eye | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park²⁵

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor of ommatidium | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park²⁵

(Whitworth et al., 2008)

HtrA2^Δ1 is a suppressor | partially of eye | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF

(Whitworth et al., 2008)

NOT Suppressor of

Statement

Reference

HtrA2^Δ1 is a non-suppressor of eye | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park^UAS.cGa

(Whitworth et al., 2008)

HtrA2^Δ1 is a non-suppressor of ommatidium | adult stage phenotype of Pink1^UAS.Tag:HA, Scer\GAL4^GMR.PF, park^UAS.cGa

(Whitworth et al., 2008)

HtrA2^Δ1 is a non-suppressor of eye phenotype of Scer\GAL4^GMR.PF, park^UAS.cGa, rho-7^UAS.cWa

(Whitworth et al., 2008)

HtrA2^Δ1 is a non-suppressor of interommatidial bristle phenotype of Scer\GAL4^GMR.PF, park^UAS.cGa, rho-7^UAS.cWa

(Whitworth et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

The climbing ability of HtrA2^Δ1 Pink1^B9 double mutants is not significantly different from the climbing ability of the Pink1^B9 single mutant.

HtrA2^Δ1 park²⁵ double mutants have dramatically enhanced defects in climbing ability compared to park²⁵ single mutants.

(Tain et al., 2009)

HtrA2^Δ1 largely suppresses the rough eye phenotype seen when Pink1^{Scer\UAS.T:Ivir\HA1} is expressed under the control of Scer\GAL4^GMR.PF.

HtrA2^Δ1 partially suppresses the rough eye phenotype seen when rho-7^Scer\UAS.cWa is expressed under the control of Scer\GAL4^GMR.PF.

Expression of park^Scer\UAS.cGa enhances the rough eye phenotype seen when rho-7^Scer\UAS.cWa is expressed under the control of Scer\GAL4^GMR.PF, resulting in severe loss of eye tissue. This phenotype is not suppressed by HtrA2^Δ1.

park²⁵ partially suppresses the rough eye and ommatidial organisation phenotypes seen when Pink1^{Scer\UAS.T:Ivir\HA1} is expressed under the control of Scer\GAL4^GMR.PF. Addition of HtrA2^Δ1 suppresses the phenotype completely.

Co-expression of Pink1^{Scer\UAS.T:Ivir\HA1} and park^Scer\UAS.cGa under the control of Scer\GAL4^GMR.PF results in a severe rough eye phenotype, which greatly exceeds that conferred when Pink1^{Scer\UAS.T:Ivir\HA1} is expressed alone. This phenotype is not suppressed in a HtrA2^Δ1 mutant background.

(Whitworth et al., 2008)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

HtrA2^Δ1 is rescued by HtrA2^+t2.5

(Yacobi-Sharon et al., 2013)

HtrA2^Δ1 is rescued by HtrA2^+t2.5

(Tain et al., 2009)

Comments

Expression of two copies of HtrA2^+t2.5 rescues the germline cell death seen in the spermatogonial cysts of HtrA2^Δ1 mutant flies. The levels of germline cell death in these flies are approximately 120% of wild type levels.

(Yacobi-Sharon et al., 2013)

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

HtrA2^Δ1

(Monteiro et al., 2023)

omi^Δ1

(Tarayrah-Ibraheim et al., 2021, Yacobi-Sharon et al., 2013)

Name Synonyms

Secondary FlyBase IDs

References (5)

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