FB2024_03 , released June 25, 2024
Allele: Dmel\ptc16
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General Information
Symbol
Dmel\ptc16
Species
D. melanogaster
Name
FlyBase ID
FBal0028506
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ptcIIW, ptcIIw109, ptc-, ptcW109
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

The premature stop codon is before the first transmembrane domain.

Amino acid replacement: ??term.

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

head capsule & cuticle | ectopic (with ptc559.1)

head capsule & cuticle | ectopic (with ptctuf-1)

Detailed Description
Statement
Reference

In ptc16/ptcD130 mutant embryos, ganglionic branches do not extend into the ventral nerve cord. Defects in the dorsal branch, elongation and in dorsal trunk thickness and convolution are also observed. In addition, the visceral branches are very often misplaced, localising more ventrally than in the wild-type.

Homozygous mushroom body gamma neuron clones show normal axon pruning.

When ptc16 somatic clones are made in a ptcL.Δloop2.RpL32 wing, anterior clones appear wild-type, clones along the anterior posterior compartment boundary form a mirror symmetric duplication of a more anterior pattern, including an ectopic wing vein 3 and triple row bristles.

All flies carrying ptctuf-1 in trans to ptc16 have severely reduced, rough eyes, a highly enlarged head vertex (ocellar triangle, fronto-orbital plate and frons), outgrowths of head cuticle and large numbers of missing, misplaced or ectopic head bristles. ptc559.1/ptc16 flies have mildly reduced eyes, a normal sized head vertex and low incidences of head cuticle outgrowths and ectopic or misplaced head bristles. ptc16 somatic clones in the head vertex region (ocellar triangle, fronto-orbital plate and frons) cause duplication of macrochaetae and an increase in the size of ocelli (occasionally the medial ocellus is split in two). Ectopic ocelli often form in lateral regions of the head vertex together with ocellar and posterior vertical bristles. In the eye discs of late third instar ptc16/ptctuf-1 larvae, apoptosis is increased in a broad swath of cells situated behind the furrow.

4% of ptcP83/ptc16 animals survive to adulthood. Survivors show fusion of wing veins L3 and L4. 11% of ptcQ67/ptc16 animals survive to adulthood. Survivors show fusion of wing veins L3 and L4.

ptcCwh1/ptc16 flies show duplication of the scutellar macrochaetae.

When ptc16 germ-line clones are induced, mutant cysts are still seen to develop in the germarium. However no ptc16 egg chambers are detected after stage 7. Somatic clones overproliferate. This overproliferation does not depend on whether their neighbouring germ-line cells are ptc+ or not.

Homozygous cells in the anterior of mosaic wing imaginal discs minimise contact with neighbouring ptc+ cells, resulting in round clones with smooth borders. Very few clones survive in the region between veins L1 and L2 in the wing. Duplications of vein L3 are often seen, but vein L4 is never disrupted in wings containing clones. Homozygous embryos retain only two isolated denticle rows per segment.

homozygous and hemizygous mutants display distortion in the costal cell and an increase in the distance between the L3 and L4 wing veins.

Clones induced in the P compartment of the abdominal tergite show no mutant phenotype. In the anterior domain of the A compartment, mutant cells develop normally in the a1 region but a2 is transformed to a1. Mutant cells develop normally in the posterior a6, but clones in a5, a4 and a3 resemble a6 (based on phenotypic and cell marker expression considerations). Some clones are more complex and become associated with a complete sequence of cuticle types arranged in reverse order. Cells in the clone secrete p3, p2 and p1 cuticle while, posterior to the clone, a5 and a6 cuticle are induced. At the anterior limit of the clone there is an ectopic P/A compartment boundary with a1 being made by wild type cells. Flanking anterior cells not in the clone become a2-like. Cells in clones have a tendency to sort out, but survivors in the middle of the segment produce hairs and bristles pointing towards the center of the clone with a zone of reversed polarity behind the clone up to several cells wide.

Clones in the posterior domain of the A compartment make a6 cuticle, and tend to sort out or back, leaving their twin wild type clone. The mutant clone is smaller and more circular than the twin.

ptcG20/ptc16 wing discs show an extension of all sensory organ precursor cells close to the A/P border, with extra sensilla induced in the Sc25, Sc4d and Sc12 clusters and extra vein 3 sensilla throughout the anterior compartment. ptctuf-1/ptc16 flies have extra bristles in the scutellum.

ptc16 ptcαTub84B.PCa wing clones that arise at a distance from the A/P boundary do not alter the adult wing pattern. The presence of the transgene does not rescue the development of clones that arise immediately anterior to the A/P boundary. Replacing one copy of ptc16 with ptcS2 gives rise to normal flies.

ptcG20/ptc16 heterozygotes display severe disorganisation and necrosis of the wing.

Heterozygotes with ptctuf-1 display a variable phenotype including overgrowth of the anterior compartment of the wing, loss of costal structures and wing vein defects and loss of scutellar bristles. Heterozygotes with ptcG20 are pupal lethal. ptctuf-1/ptc16 heterozygotes display severe outgrowth of the anterior compartment of the wing disc, loss of costal structures, duplications or plexations of veins 1 and 2, increase of the distance between veins 3 and 4 and increase in the number of scutellar bristles. The combination ptcG20/ptc16 is semi-viable. Wings show overgrowth of the anterior compartment, partial or complete loss of vein 2 and plexation of veins 1 and 3. Extra bristles appear on the notum and there are morphological alterations in the legs.

homozygous lethal

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

ptc16/ptcG20 has phenotype, suppressible by fuJ

ptc16/ptcG20 has phenotype, suppressible | partially by dppd5/dppd12

Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

ptc16/ptctuf-1 is a suppressor of eye phenotype of hhbar3

ptc16 is a suppressor of germarium phenotype of fs(1)YbM104-3

ptc16 is a suppressor of germline stem cell phenotype of fs(1)YbM104-3

ptc16 is a suppressor of egg chamber phenotype of fs(1)YbM104-3

Other
Additional Comments
Genetic Interactions
Statement
Reference

The axon pruning defect of Atg61 mushroom body gamma neuron clones is significantly suppressed if the neurons are also homozygous for ptc16.

ptc16/+ ; tow754/tow754 flies show a slight increase in the mean number of The number of campaniform sensilla (CS) along wing vein 3 compared to wild type, and the percentage of wings with aberrant CS numbers is also increased. The intervein area between veins 3 and 4 is also increased.

ptc16/+ enhances the increase in the number of campaniform sensilla (CS) along wing vein 3 seen in Su(fu)LP homozygotes (both the average number of CS and the fraction of wings with aberrant numbers of CS is increased).

The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is still seen if the clones are induced in a stan3/stanE59 background, as occurs in clones induced a wild-type background.

The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is still seen if the clones are induced in a fzunspecified background, as occurs in clones induced a wild-type background.

The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is still seen if the clones are induced in a dsunspecified background, as occurs in clones induced a wild-type background.

The reversal of cell polarity phenotype that is seen in cells posterior to clones in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are doubly mutant for ptc16 and Df(2R)enE is not seen if the clones are induced in a dsunspecified stan3/stanE59 double mutant background instead of a wild-type background.

Clones of cells in the anterior compartment of the dorsal epidermis of the adult abdomen (in the tergite) where the clones are triply mutant for ptc16, Df(2R)enE and stanE59 and have been induced in a dsunspecified background do not result in a reversal of cell polarity in cells surrounding the clone.

When biomb-3198 ptc16 double homozygous clones are made in the anterior compartment of the abdominal segment. These clones makes segmental region anterior 6 (a6) cuticle, like ptc16 clones, but reverse polarity in the front half of the clone as do biomb-3198 clones.

fs(1)YbM104-3 homozygous ovarioles that contain ptc16 clones contain functional germaria and an average of 4.6 post-germarial egg chambers. Some ovarioles contain up to seven egg chambers. However these germaria are somewhat rudimentary and comparable in size and morphology to old wild-type germaria with only one remaining germline stem cell.

ptc16 ci94 double mutant clones in the anterior of the wing disc have "wiggly" boundaries indistinguishable from wild-type control clones. ptc16 ci94 double mutant clones in the wing show the same features as ci94 single mutant clones. ci94 ptc16 double mutant embryos show a higher degree of naked cuticle compared with ci94 single mutants. They also differ from ptc16 single mutant embryos. ci94 ptc16 double mutant embryos derived from ci94 ptc16 female germline clones have the same phenotype as ci single mutant embryos. The addition of hhAC does not aggravate the ptc16 mutant phenotype.

Double mutant clones of ptc16 and Df(2R)enE induced in the a2 region of the A compartment behave as ptc16 clones and make a1 cuticle. In the rest of the compartment clones make dusky a5 as opposed to clear a6-type cuticle. No clones make P-type cuticle. Single clones of ptc16 and Df(2R)enE in the A compartment can make both a1 and a5 cuticle, and reorganize polarity within and behind the clone. The results are slightly different for A6 than for more anterior segments: cuticle made by clones resembles the lightly pigmented cuticle found just posterior to a5 in segment A6. Pupal mutant clones of ptc16 and Df(2R)enE appear exactly like Df(2R)enE clones.

Clones mutant for ptc16 and Df(2R)enE induced in the posterior domain of the anterior compartment produce a5 cuticle. Clones induced before 12 hours APF reveal that the mutant cells have different affinities than those around them, judging from the shape of, and cell density within, the clone. This different affinity is graded across the segment. In the posterior domain of the A compartment, the later the induction, the further anterior the clone, and the more anterior the clone, the more circular its shape and smaller its size. In the posterior domain of the A compartment twin clones are oriented with mutant posterior to wild type. In the anterior domain of the A compartment twin clones are oriented with mutant anterior to wild type. Some clones span both anterior and posterior domains of the A compartment. Clones mutant for ptc16 and Df(2R)enE induced in the posterior compartment in the larval period or earlier rarely survive. Survivors are anteriorly located, produce a5 cuticle, and most fuse with the anterior compartment, a5 cuticle. Clones mutant for ptc16 and Df(2R)enE induced in the posterior compartment in the pupal period produce a5 cuticle and lie anterior to the twin clone. The clone and its twin can be separated by several cell diameters. The mutant clone is more circular and smaller that the twin. Clones mutant for ptc16 and Df(2R)enE induced in the posterior compartment in the pupal period after 12 hours APF are small and only partially transformed to A identity.

fuJ; ptcG20/ptc16 flies are viable and show a fu phenotype, and the ptc phenotype is rescued, although occasionally incompletely.

Partial rescue of the ptc phenotype is seen in dppd12 ptcG20 / dppd5 ptc16, increased bristle numbers on legs, antennae and notum are lower and reduced overgrowth of pharate adult legs.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially complements
Partially rescued by
Comments

30% of the expected number of ptck02507/ptc16 transheterozygotes emerge. Escapers are viable and fertile.

ptcαTub84B.PCa can rescue ptc16/ptcS2 mutants to adulthood, adults have normal wings.

The lethality seen in combination with ptcG20 can be rescued by ptchs.PSa.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (64)