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General Information
Symbol
Dmel\Pkn06736
Species
D. melanogaster
Name
FlyBase ID
FBal0008115
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
PknP, l(2)06736
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{PZ} is inserted in an intron whose 5' end is located 21bp downstream of the putative ATG start codon of the Pkn-coding sequence.

Insertion components
P{PZ}Pkn06736
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Whereas wild-type larval neuroblasts during asymmetric cell division expand the apical cortex during anaphase, the Pkn06736/Df(2R)w73-1 mutant neuroblasts first expand the basal cortex which subsequently retracts and then the apical cortex is enlarged, causing a temporarily inverted asymmetric anaphase figure followed by a symmetric one and finally normal asymmetric figure. The cell curvature along the apical-basal neuroblast cortex from early anaphase to telophase is also abnormal in Pkn06736/Df(2R)w73-1 neuroblasts: While wild-type cells show a cortical ingression (negative curvature) in a basally shifted position at early anaphase stage, this ingression develops into a pronounced cleavage furrow but remain at approximately the location. In contrast, the mutant neuroblasts initiate furrowing close to the apical cortex and this ingression then shifts basally during anaphase.

Even prior to anaphase, during metaphase, the Pkn06736/Df(2R)w73-1 neuroblasts display significant cell shape deformation of the apical cortex - both positive and negative changes in curvature while in wild-type neuroblasts the curvature change very little during metaphase.

This abnormal shape dynamics is underpinned by spatiotemporal aberrations in myosin localization pattern and activity.

Egg length is significantly reduced in Pkn06736/Pkn06736 female germline clones.

During nurse cell dumping, egg chambers mutant for Pkn06736/Pkn06736 show increased nurse cell-to-oocyte membrane collapse, leading to abnormal presence of ring canals, border cells and/or nurse cell nuclei in the oocyte cytoplasm.

Females with Pkn06736/Pkn06736 germline clones show intermediate abnormal accumulation of F-actin in nurse cells of stage 10 egg chambers.

No adult homozygotes emerge. 10% of homozygous embryos show a dorsal closure phenotype. Germline clones produced mutant embryos, about 55% of which showed defects in dorsal closure. No defects in patterning or in the central and peripheral nervous systems or somatic muscles were found. When embryos from germline clone mothers are examined for cell shape, despite apparently normal leading edge cell stretching, all epidermal cells adopt an unstretched polygonal shape.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

Pkn06736 has lethal phenotype, non-suppressible by Pkn::Rokhs.PB

Pkn06736 has lethal phenotype, non-suppressible by Pak::Pknhs.PB

Pkn06736 has lethal phenotype, non-suppressible by Pak::Pkc53Ehs.PB

Pkn06736 has lethal phenotype, non-suppressible by Pkc53E::Rokhs.PB

Suppressor of
Statement
Reference

Pkn06736/Pkn[+] is a suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressor of
Statement
Reference

Pkn06736/Pkn[+] is a suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

Additional Comments
Genetic Interactions
Statement
Reference

Expression of Pkc53E::Pknhs.PB (using a reduced heat shock regime of 15 minutes per day) can partially rescue the lethality of Pkn06736.

Pkn06736/+ suppresses the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is increased from 9% to 27%).

Pkn3 shows no interaction with Sb70 or Sb63b (assayed in terms of a malformed leg phenotype). Pkn06736 shows a weak dominant enhancement of leg malformation in Sbsbd-201/Sbsbd-1 flies.

When Pkn06736 germline clone mothers are crossed with bsk1 or Rho172R fathers, 76% or 68% of the embryos showed an identical dorsal closure phenotype, respectively, an enhancement of the dorsal closure phenotype caused by Pkn06736 germline clones alone.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Complements: l(2)0365903659. Complements: l(2)0384503845. Complements: l(2)45Bck05611a. Complements: Pknk11209. Complements: PknrG232. Complements: l(2)s1976s1976.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (14)