FB2024_03 , released June 25, 2024
Allele: Dmel\pkpk-sple-13
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General Information
Symbol
Dmel\pkpk-sple-13
Species
D. melanogaster
Name
FlyBase ID
FBal0060943
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
pkpk-sple13, pk-sple13, pk13
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Lesion present between 40.2 and 66.2kb downstream of zero (zero being 973bp proximal to the pk transcription start site.).

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 0 )
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

Overall length of the tracheal dorsal trunk is normal in pkpk-sple-13/pkeq stage 16 embryos.

Homozygous adults show defects in ommatidial patterning, with ommatidia having random orientation and chirality.

Homozygous clones in the pupal wing (23 hours after puparium formation) do not affect polarity of trichomes in surrounding wild-type tissue.

pkpk-sple-13 somatic clones in the adult abdomen have disturbed polarity - usually a 'whorl' of hairs. This effect is cell autonomous.

Mutant animals display a planar cell polarity eye phenotype: misrotations and random chirality with an associated loss of the mirror symmetry line, the equator, at the dorsoventral midline. Chirality defects appear to be associated with a mutant R4 precursor.

57.8% of ommatidia in pkpk-sple-13/pksple-1 mutant somatic clones in the eye are normal. 0.6% have rotated ommatidia, 41.6% have chirality defects, none are achiral (0% unscorable). 53.0% of ommatidia in homozygous mutant somatic clones in the eye are normal. 4.6% have rotated ommatidia, 41.9% have chirality defects, 0.5% are achiral (0% unscorable).

85% of homozygous somatic clones in the wing exhibit cell autonomy, though about 15% display a clear domineering non-autonomy. This is not restricted to large or early induced clones.

Causes no embryonic phenotype even when homozygous mutant embryos develop from homozygous mutant mothers. Has a weak polarity phenotype in the wing, notum, abdomen, eye and legs. In the wing, shows a slight effect on triple-row bristle orientation and gently curved hair polarity vectors. In the eye a mixture of chiral forms of ommatidia are seen. Some ommatidia fail to rotate properly, resulting in imperfections in the hexagonal stacking and a slightly rough eye phenotype. Some ommatidia are aligned at 60o to the equator and some show anterior-posterior axis reversals. The T3 and T4 segments carry medial duplications of the proximal and distal joint structures, with the middle of each segment deleted. This results in alternating reversed-proximal and reversed-distal tarsal joint structures with half the length of a normal segment. T5 is unaffected. Denticle belt morphology and denticle orientation remains wild-type. Wings in pkpk-sple-13/pk30 flies show a phenotype stronger than pkpk-sple-13/pkpk-sple-13 and weaker than pk30/pk30.

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

pkpk-sple-13 has wing hair phenotype, non-suppressible by dshhs.PA

Enhancer of
Statement
Reference

pk[+]/pkpk-sple-13 is an enhancer of wing hair phenotype of dco2/dco5B2.6

pkpk-sple-13/pkpk-sple-13 is an enhancer of trichome & adult abdomen phenotype of fzUAS.cSa

NOT Enhancer of
Statement
Reference

pk[+]/pkpk-sple-13 is a non-enhancer of eye phenotype of Nab2EP3716, Scer\GAL4GMR.PU

pkpk-sple-13/pkpk-sple-13 is a non-enhancer of trichome & adult abdomen phenotype of fz21

Suppressor of
Statement
Reference

pkpk-sple-13 is a suppressor of wing hair phenotype of dshhs.PA

pkpk-sple-13 is a suppressor of wing vein phenotype of Nnd-3

pkpk-sple-13 is a suppressor of wing phenotype of Nnd-3

NOT Suppressor of
Statement
Reference

pk[+]/pkpk-sple-13 is a non-suppressor of eye phenotype of Nab2EP3716, Scer\GAL4GMR.PU

pkpk-sple-13 is a non-suppressor of ommatidium phenotype of ecspok

pkpk-sple-13/pkpk-sple-13 is a non-suppressor of trichome & abdomen | cell non-autonomous | somatic clone phenotype of fz15

pkpk-sple-13/pkpk-sple-13 is a non-suppressor of trichome & adult abdomen phenotype of fz21

Other
Additional Comments
Genetic Interactions
Statement
Reference

Vangstbm-6, dgo380, pkpk-sple-13 and dsh3, Vangstbm-6, dgo380, pkpk-sple-13 triple and quadruple heterozygotes exhibit mild wing trichome orientation defects in proximal regions.

Flies expressing Mks1GD9100 under the control of Scer\GAL4en-e16E in a pkpk-sple-13/+ genetic background display wild-type wing hair polarity.

Flies expressing CG15283GD13108 under the control of Scer\GAL4en-e16E in a pkpk-sple-13/+ genetic background display wild-type wing hair polarity.

pkpk-sple-13/+ suppresses the ommatidial over-rotation phenotype which is caused by expression of nmoScer\UAS.cUa under the control of Scer\GAL4hs.2sev.

The ommatidial rotation defects observed in ecspok hemizygous adult eyes are not suppressed by pkpk-sple-13/+.

pkpk-sple-13 fz21/fz21 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes towards the clone, as occurs with fz21/fz21 single mutant clones in the pupal wing.

pkpk-sple-13 Vangstbm-6/Vangstbm-6 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone, as occurs with Vangstbm-6/Vangstbm-6 single mutant clones in the pupal wing.

dgo380 pkpk-sple-13/pkpk-sple-13 clones in the pupal wing (32 hours after puparium formation) do not affect polarity of trichomes in surrounding wild-type tissue.

The planar polarity phenotype in the abdomen of fz21/fz21 flies is largely unaffected when the whole animal is pkpk-sple-13/pkpk-sple-13.

When fzScer\UAS.cZa; Scer\GAL4hh-Gal4 flies are pkpk-sple-13 homozygous, the zone of repolarisation straddling the anterior-posterior compartment boundaries in adult abdominal segements is enlarged, but otherwise unchanged.

The addition of dshhs.PA to pkpk-sple-13 animals has no effect on the pkpk-sple-13 wing hair polarity phenotype.

Completely suppresses the wing phenotypes (thickened veins and wing-edge loss) of Nnd-3 flies.

Does not alter the eye tissue polarity phenotype produced by fzScer\UAS.cAa expressed under the control of Scer\GAL4hs.2sev.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of pkAct5C.T:Hsap\MYC,T:Ivir\HA1,T:Zzzz\PSP.CS fully rescues the wing planar polarity phenotype seen in pkpk-sple-13 mutant wings.

Expression of pkAct5C.pk.T:Avic\GFP-EGFP fully rescues the wing planar polarity phenotype seen in pkpk-sple-13 mutant wings.

Expression of pkAct5C.pk.T:Avic\GFP-EGFP partially rescues the eye planar polarity phenotype seen in pkpk-sple-13 mutant flies. The misrotation is rescued, but the chirality defects are still present.

Expression of pkΔCaaX.Act5C.pk.T:Avic\GFP-EGFP fails to rescue the wing planar polarity phenotype seen in pkpk-sple-13 mutant wings.

Expression of pkΔCaaX.Act5C.pk.T:Avic\GFP-EGFP partially rescues the eye planar polarity phenotype seen in pkpk-sple-13 mutant flies. The misrotation is rescued, but the chirality defects are still present.

Expression of pkAct5C.sple.T:Avic\GFP-EGFP fully rescues the planar polarity phenotypes seen in pkpk-sple-13 mutant eyes and legs. The wing planar polarity phenotype is altered but not rescued; the trichomes point proximally and towards vein 3, as is seen in pk1 mutant flies.

Expression of pkΔCaaX.Act5C.sple.T:Avic\GFP-EGFP partially rescues the planar polarity phenotypes seen in pkpk-sple-13 mutant eyes and legs. 9% of ommatidia are still inverted but the misrotation phenotype is completely rescued.

Expression of pkΔCaaX.Act5C.sple.T:Avic\GFP-EGFP has no effect on the planar polarity phenotype seen in pkpk-sple-13 mutant wings.

pkAct5C.pk can rescue the wing planar polarity defects seen in pkpk-sple-13 homozygotes. Expression at 16 and 20 hours after puparium formation (APF) results in only negligible polarity defects in the rescued wings, and expression at 24 and 28 hours APF provides partial rescue.

pksev.sple.PS rescues the ommatidial polarity defects of pkpk-sple-13 homozygotes.

Clones expressing fzScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Act5C.PI in a pkpk-sple-13/pkpk-sple-13 background result in non-clonal cells pointing their trichomes away from the clone. This effect extends 8-9 cells from the clone boundary. This effect is still seen if the clones are also mutant for dgo380, but in this case the effect only extends 5-6 cells from the clone boundary.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (47)