FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\pk1
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General Information
Symbol
Dmel\pk1
Species
D. melanogaster
Name
FlyBase ID
FBal0013838
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
pkpk1, pkpk
Key Links
Genomic Maps

Mutagen
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

Amino acid replacement: P38T.

Nucleotide substitution: C902A.

Amino acid replacement: S634P.

Nucleotide substitution: T2690C.

Tirant insertion in the 5'UTR, along with two missense mutations (P38T and S634P).

Lesion present between 0 and 2.2kb 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
Nucleotide change:

C7209053A

Amino acid change:

P38T | pk-PA; P104T | pk-PB; P374T | pk-PC

Reported amino acid change:

P38T

Comment:

P38T mutation relative to pk-PA. One of two amino acid changes in mutant. There is also a Tirant insertion in the 5' UTR.

Nucleotide change:

T7221827C

Amino acid change:

S634P | pk-PA; S700P | pk-PB; S970P | pk-PC

Reported amino acid change:

S634P

Comment:

S634P mutation relative to pk-PA. One of two amino acid changes in mutant. There is also a Tirant insertion in the 5' UTR.

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

In pk1 testes the number of normal individualization complexes (ICs), abnormal ICs and waste bags is similar to controls.

pk1/+ flies do not exhibit significantly increased bang sensitivity, nor a significant difference in threshold required to trigger seizure discharges or spiking activity in an electroconvulsive stimulation paradigm, as compared to wild type. pk1/+ larvae display defective vesicle transport in segmental nerves, with significant decreases in both anterograde and retrograde vesicle velocities and an increase in vesicle pause duration, as compared to controls.

pk1/pk1 mutants exhibit significantly reduced viability, as compared to wild type.

The hexagonal packing of intervein cells, which usually occurs between wing development stage P2B (when the first morphological signs of veins appear (FBrf0005070), and the middle of P2C (before hair formation (FBrf0005070)) is disrupted in pk1/pk1 flies.

pk1 somatic clones in the adult abdomen have disturbed polarity - usually a 'whorl' of hairs. This effect is cell autonomous.

Mutants show no significant disruption of ovarian morphology.

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. The clones show the same polarity as cells in equivalent positions in entirely mutant pk1 wings.

Causes no embryonic phenotype even when homozygous mutant embryos develop from homozygous mutant mothers. Causes an extreme polarity phenotype in the wing and notum. The triple row bristles are reversed along the anterior margin and a whorl in the wing hairs is seen near the tip of vein 2. Shows a low penetrance doubled hair phenotype. Eyes are wild-type. Tarsi are wild-type. Denticle belt morphology and denticle orientation remains wild-type. Within pk1 somatic clones in the wing the mutant polarity pattern is generally cell autonomous, with only occasional short range non-autonomous disruption of polarity in wild-type cells adjacent to the proximal and lateral margins of a clone. There is no clear pattern to the position of such clones, but small peninsulas of wild-type tissue surrounded by pk1 tissue tend to adopt the mutant polarity pattern. Smaller clones, induced later than 72-96 hr, do not alter the polarity of adjacent tissue. Wild-type hairs are oriented towards the clone as though it is acting as a polarity 'sink'.

Homozygotes in combination with P{hsfzI} heat shocked to induce a strong hsfz-late phenotype fail to suppress the multiple hair cell (MHC) phenotype.

Most wing cells of homozygous flies form a single hair. Homozygous flies have disruptions in the pattern of wing hair polarity. The prehair initiation site is moved to near the cell centre in pupal wing cells. Double mutants of pk1 with in1, fy2 or mwh1 resemble in1, fy2 or mwh1 single mutants respectively.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

pk[+]/pk1 is a suppressor of abnormal planar polarity phenotype of dsh1

Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference

pk1 has phenotype, non-enhanceable by Glidv5

NOT suppressed by
Statement
Reference

pk1 has phenotype, non-suppressible by Glidv5

Enhancer of
Statement
Reference

pk[+]/pk1 is an enhancer of wing cell | adult stage | heat sensitive phenotype of shi1

pk1 is an enhancer of ommatidium phenotype of Vangsev.PR

pk1 is an enhancer of ommatidium phenotype of Vangstbm-153

pk1 is an enhancer of wing hair & 1st posterior cell phenotype of inII53

Suppressor of
Statement
Reference

pk[+]/pk1 is a suppressor of ommatidium phenotype of dsh1

pk1 is a suppressor of phenotype of Vang14-11

pk1 is a suppressor of phenotype of Vang11-3

pk1 is a suppressor of phenotype of VangA3

pk1 is a suppressor of wing hair phenotype of VangTbs42

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The formation of holes in wings due to temperature shift of shi1/shi1 animals during pupal stages is moderately enhanced by pk1/+.

The planar cell polarity phenotype seen in the eyes of dsh1/Y flies is partially suppressed by pk1/+.

Glidv5/Glidv5, pk1/pk1 animals exhibit an additive wing hair phenotype.

fz23 homozygous clones in pk1 wings, exhibit domineering cell non-autonomy where the direction of the non-autonomy is no longer distal. For these clones the domineering cell autonomy is in the same direction as local hair polarity.

Vang is epistatic to pk; double mutants of VangTbs42, VangA3 or VangA5 with pk1 show a fz-in group phenotype, possible less severe than for the Vang single mutant. Dominantly suppresses the wing basal cell 1 swirl phenotype of Vang alleles. VangTbs42, pk1 double mutants show an increase in multiple wing hair cells over either single mutant.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Not rescued by
Comments

pk1/pksple-1 flies do not exhibit significantly increased bang sensitivity, nor a significant difference in threshold required to trigger seizure discharges or spiking activity in an electroconvulsive stimulation paradigm, as compared to wild type.

Expression of pkAct5C.pk.T:Avic\GFP-EGFP fully rescues the wing planar polarity phenotype seen in pk1 mutant wings.

Expression of pkΔCaaX.Act5C.pk.T:Avic\GFP-EGFP fails to rescue the wing planar polarity phenotype seen in pk1 mutant wings.

Images (1)
Stocks (18)
Notes on Origin
Discoverer

Ives, Nov. 1938.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (31)