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.).
C7209053A
P38T | pk-PA; P104T | pk-PB; P374T | pk-PC
P38T
P38T mutation relative to pk-PA. One of two amino acid changes in mutant. There is also a Tirant insertion in the 5' UTR.
T7221827C
S634P | pk-PA; S700P | pk-PB; S970P | pk-PC
S634P
S634P mutation relative to pk-PA. One of two amino acid changes in mutant. There is also a Tirant insertion in the 5' UTR.
trichome & adult abdomen | somatic clone | cell autonomous
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.
pk1 is an enhancer of abnormal planar polarity phenotype of Vangsev.PR
pk1 is an enhancer of abnormal planar polarity phenotype of Vangstbm-153
pk[+]/pk1 is a suppressor of abnormal planar polarity phenotype of dsh1
fz23, pk1 has abnormal planar polarity | somatic clone | cell non-autonomous phenotype
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
fz23, pk1 has wing | somatic clone | cell non-autonomous phenotype
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.
pk1 is rescued by pkAct5C.pk.EGFP
pk1 is not rescued by pkΔCaaX.Act5C.pk.EGFP
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.
Ives, Nov. 1938.