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General Information
Symbol
Dmel\DroncI29
Species
D. melanogaster
Name
FlyBase ID
FBal0190283
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DroncL29
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C9969044T

Amino acid change:

Q53term | Dronc-PA

Reported amino acid change:

Q53term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: ?53term.

Amino acid replacement: Q53term.

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
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
Detailed Description
Statement
Reference

DroncI29 homozygotes do not show any obvious eye phenotype, as compared to controls.

DroncI29/DroncL32 transheterozygotes exhibit a significant increase in the proportion of hyperplastic testes as compared to controls; these testes exhibit a significant decrease in necrosis at their apical tip (as shown by the number of spermatogonial cysts bearing Propidium Iodine-positive or TUNEL-positive cells), as compared to controls. During spermatogenesis, cystic bulges and waste bags are largely absent and actin investment cones in the individualization complex are uncoordinated, as compared to controls.

Homozygous NcI29 escapers are unhealthy and do not survive long after eclosion. The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed. Highly variable numbers of bursCCAP neurons are seen at 3-5 days.

NcI24/NcI29 mutant males exhibit ~40% less spermatogonial cyst death compared to controls.

NcI29/NcL32 mutant males exhibit ~60% less spermatogonial cyst death compared to controls.

Adult eyes mosaic for NcI29 are predominantly white, indicating that NcI29 mutant cells (that are white) proliferate faster than wild-type cells (that are red) and out-compete them.

NcI29 mutant eye clones are significantly larger than their wild-type twin spots.

NcI29 mutant eye clones induce ectopic cell proliferation posterior to the second mitotic wave in the eye-antennal disc.

NcI29 mutant eye clones exhibit extra ommatidial pigment cells in the pupal retina.

NcI29 homozygotes and NcI29/Nc51 transheterozygotes exhibit a delay in vCrz neuron apoptosis. At 7 hours after puparium formation 75% vCrz neurons are still present although these all die by 48 hours after puparium formation.

Ovaries containing homozygous germline clones have slight defects in programmed cell death in mid-oogenesis, with some egg chambers having condensed nurse cell nuclei but no somatic follicle cells. 10% of stage 14 egg chambers contain persisting nurse cell nuclei.

Salivary glands are degraded by 24 hours after puparium formation (as occurs in wild-type controls) in NcI24/NcI29 mutants that develop normally.

100% of NcI29/NcI24 male escapers have a rotated genitalia defect. 100% of NcI29/NcI24 adult escapers have a ballooned wing phenotype.

NcI29 mutants display severe defects during the spermatid individualization process. The cystic bulges are frequently reduced in size or appear flat due to a failure in the appropriate collection of the cytoplasm of the spermatids . The retained cytoplasm is clearly visualized as a trail along the entire length of what was supposed to have been the post-individualized portion of the spermatids. Frequently a large portion of the spermatid cytoplasm is retained in a 'mini' cystic bulge structure, which often contains part of the individualization complex. Waste bags are also reduced in size.

Nc51/NcI29 mutants exhibit a delay in programmed cell death in Crz-expressing neurons in the ventral nerve cord during pupation.

Homozygous clones in the eye result in an excess of interommatidial cells in the retina at 42 hours after puparium formation compared to wild type. Mutant clones at the edge of the eye have extra perimeter ommatidial cells that are never eliminated.

Homozygous escapers have wings that are less transparent than normal and are curved. Homozygous embryos derived from females carrying homozygous germline clones have a head defect. These embryos show a substantial reduction in the number of apoptotic cells compared to wild type. Stage 17 embryos contain additional midline glia cells compared to wild type. There is a general enlargement of the central nervous system in these embryos. Each chordotonal organ cluster contains on average about 3 additional neurons.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

DroncI29 has neuron phenotype, enhanceable by Dcp-1Prev1

Enhancer of
Suppressor of
Statement
Reference
NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The small eye phenotype resulting from the cell death induced by expression of hidGMR.PG is partially suppressed by combination with DroncI29.

DroncI29 largely suppresses the increase in apoptosis seen in Vps43B1 mutant eye disc clones. The reduction in R8 photoreceptor number is also suppressed.

Vps43B1 suppresses the increase in photoreceptor number seen in shi7C7 mutant eye disc clones, with the double mutants showing the photoreceptor loss seen in Vps43B1 mutants alone. The same is seen in a DroncI29 mutant background.

shiFL54 does not suppress the photoreceptor loss seen in Vps43B1 mutant eye disc clones (in which cell death has been prevented using DroncI29).

DroncI29/DroncI29 suppresses increased cell death seen in Ipk220B/Ipk220B third instar larval wing discs.

One copy of DroncI29 slightly suppresses the eye roughness seen when SRm160GE25979 is expressed under the control of Scer\GAL4GMR.PU.

Dcp-1Prev1; NcI29 double mutants exhibit an arrest of vCrz programmed cell death with all 16 vCrz neurons retained at 7 and 16 hours after puparium formation, compared to apoptosis of these neurons in wild-type controls.

Induction of NcI29 third instar larval eyes disc clones blocks the cell death seen when p53GUS.PB is expressed under the control of Scer\GAL4GMR.PU. However the reduction in R7 photoreceptors is not rescued.

Dcp-1Prev1 ; NcI24/NcI29 IceΔ1 triple mutant larvae undergo cell death with morphology similar to the midgut of wild-type animals when analysed from -4 to -1 hours relative to puparium formation.

dream4 ; NcI24/NcI29 IceΔ1 triple mutant larvae show high levels of TUNEL staining at -4 to -1 hours relative to puparium formation, suggesting that they are undergoing cell death.

Females containing dream4 ; NcI29 double homozygous germline clones are fertile, but their ovaries contain 46% of mid-stage egg chambers with missing follicle cells and large surviving nurse cells. Many of these egg chambers contain excessive numbers of nurse cells. There is also an increase in mid-stage egg chambers containing condensed nurse cell nuclei but lacking follicle cells. 21% of stage 14 egg chambers contain persisting nurse cell nuclei.

No significant defects is seen in the egg chambers of females containing dream2/dream4 ; NcI29 double homozygous germline clones.

The persistence of salivary gland tissue that is seen at 24 hours hours after puparium formation when Pi3K92EScer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4fkh.PH is significantly enhanced if the animals are also carrying NcI24/NcI29.

While 59% of Scer\GAL4Act5C.PI>wgScer\UAS.cLa prothoracic leg discs form a blastema, only 15% of Scer\GAL4Act5C.PI>wgScer\UAS.cLa, NcI29 legs form a blastema.

Xenogenetic Interactions
Statement
Reference

NcI29/+ suppresses the increase in the number of TUNEL-positive cells seen in the wing discs in larvae expressing Rcom\RAcs2.Scer\UAS under the control of Scer\GAL4en-e16E at 30[o]C. It also largely rescues the non-autonomous increase in BrdU incorporation which is seen in the non-expressing compartment in discs expressing Rcom\RAcs2.Scer\UAS under the control of Scer\GAL4en-e16E at 30[o]C. NcI29/+ does not rescue the autonomous or the non-autonomous reduction in wing area caused by expression of Rcom\RAcs2.Scer\UAS under the control of Scer\GAL4en-e16E.

'Undead' Scer\GAL4en-e16E>WScer\UAS.cYa, BacA\p35Scer\UAS.cHa cells in the posterior of the wing disc show no overgrowth phenotype in a NcI29 background.

Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

Both the significant proportion of hyperplastic adult testes and the increased necrosis at the apical tip of the testes observed in DroncI29/DroncL32 transheterozygotes are rescued by the expression of Droncpro.Scer\UAS, Droncpro.C-A.Scer\UAS, DroncΔN.Scer\UAS, or DroncΔN.C-A.Scer\UAS, but not DroncCARD.Scer\UAS, under the control of Scer\GAL4nos.PU. The significant proportion of hyperplastic adult testes is also rescued by the expression of either DroncWT.5'3'UTR or DroncC-A.5'3'UTR.

The sperm individualization defects observed in DroncI29/DroncL32 transheterozygotes are not rescued by the expression of either DroncWT.5'3'UTR or DroncC-A.5'3'UTR.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Selected as: a recessive suppressor of the WGMR.PG eye ablation phenotype.

Selected as: a mutant that recessively suppresses the eye ablation phenotype caused by eye-specific overexpression of W.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (35)