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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ptcIN108, ptcIN, ptc1N108
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Nucleotide change:


Amino acid change:

S809N | ptc-PA

Reported amino acid change:



Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Amino acid replacement: S809N.

0.2 kb insertion at position +165.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
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 ptctuf-1)

Detailed Description

ptchdl animals transheterozygous for ptc9 are viable with lowly penetrant headcase defects and show lowly penetrant locomotor defects in adulthood.

Brains from ptchdl/ptc9 transheterozygous adults with severe locomotor defects show presence of lamellar inclusions and/or membranous material in neurons that are rarely present in either wild-type, young mutants or older mutant flies that do not display locomotor defects.

ptc9 embryos show a mirror-image duplication of the anterior portion of each denticle belt.

Stage 15 ptc9 embryos have 34 genital disc precursor cells, while wild type embryos have only 22 at this stage. There is no evidence of additional cell proliferation in the ptc9 genital disc precursor cells.

Homozygous embryos have epidermal defects.

Mutant animals exhibit separated nerve roots and dendritic fields in the embryonic motor system, as in wild type.

All flies carrying ptctuf-1 in trans to ptc9 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/ptc9 flies have normal sized eyes and head vertex and a low incidence of ectopic or misplaced head bristles. They also occasionally lack one or both antennae.

100% of ptchdl/ptc9 transheterozygotes show head capsule defects.

Mutant embryos have an increase in larval eye neurons and optic lobe precursors.

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

Abdominal denticle belts of mutant embryos show mirror image symmetry and only denticle types 1 and 2 are present. There is an ectopic groove in each segment.

The gnathal lobes are reduced in mutant embryos.

Polarity reversals are seen at the anterior and posterior of each denticle belt. Cells in the middle of each belt make unusually shaped denticles.

When in a wgl-17, wgScer\UAS.cLa, Scer\GAL4en-e16E background the extent of naked cuticle anterior to the Scer\GAL4en-e16E-driven wg source is narrower than in wgl-17, wgScer\UAS.cLa, Scer\GAL4en-e16E, ptc+.

Homozygotes lack RP2 neurons.

Homozygous mutants lack RP2 and RP2 sibling neurons. Double mutants with gsb525 exhibit duplicated RP2 and RP2 sibling neurons.

Homozygous embryos show duplications of the first and second rows of denticles.

Stage 11 embryos exhibit normal segmental organisation of the dorsal median cells.

Antagonizes the loss of 1o and 2o cell types found in hh mutants. In single mutants the 3o cell type is missing in the dorsal epidermis.

Mirror image transformation of the middle third of the segment into the anterior-most, leading to apodeme duplication and lateral muscle compression. The presence of ectopic segment borders at the parasegment level is translated into a two-tiered structure of the apodemes in one major row which does not affect βTub56D gene induction.

ptc9; ciD double mutants have features of both single mutants; naked cuticle is deleted and segment borders are duplicated. ptc9; ciCe-2 double mutants phenotypically resemble ciCe-2 single mutants; naked cuticle is deleted and the ventral surface consists of a lawn of denticles.

Larvae show no proventricular defects.

Coordinate mutant.

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. ptctuf-1/ptc9 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. Heterozygotes with ptcG20 are semi-viable, individuals display overgrowth in the anterior compartment of the wing and wing venation defects. P{HSptc.S} construct partially rescues the lethality and wing and wing venation defects. There are also increased numbers of bristles on the legs, notum and antennae and an increase in number of male sex comb teeth. Pharate adult legs are overgrown. The combination ptcG20/ptc9 is pupal lethal, pharate adult escapers display increase in numbers of bristles on the notum, legs and antennae and number of teeth in the male sex comb and overgrowth of legs.

Df(2R)enE ptc9 clones rescue the cell proliferation defect of Df(2R)enE clones, proliferation is induced both within the clones (posterior and anterior) and in surrounding wild type cells.

Nondefective in gonad assembly.

Mutant embryos have abnormal naked cuticle and row-1 and row-2-type ventral denticles.

Acts as a dominant suppressor of the eye phenotype of homozygous hhts2.

An ectopic stripe of hh expression appears in each segment of the embryo.

Homozygous embryos have extra parasegmental grooves in a similar position to the tracheal pits.

Cuticle ventral pattern resembles that of wg individuals: abdominal segments are covered in denticles.

Does not interact with RpII140wimp maternal effect.

Failure of head involution, lack of thoracic belts and square-shaped, mirror symmetrical abdominal belts.

ptc9 embryos had normal wg and arm protein distribution during midembryonic stages but changes were seen in protein accumulation at later stages.

Transformation of cells in the middle section of each segment so that they form pattern elements characteristic of cells at the segment or parasegment border.

A complex pattern of cell fate alterations results in specific epidermal defects.

ptc mutant embryos have Keilin's organs, but these often have four or more sensory hairs rather than the normal three. ptc9/ptcG12 and ptc9/ptcS2 embryos grew in in vivo culture, producing implants containing larval gut, Malpighian tubule, fat body, salivary gland, brain and imaginal discs. The discs tended to grow as a mass of merged sheet of material. Metamorphosed implants produced adult cuticular structures derived from the eye-antenna, leg and wing discs.

Mirror image duplications of all segment boundaries.

homozygous lethal

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

ptc9 has decreased cell number | embryonic stage phenotype, non-suppressible by enE

NOT Enhancer of
Suppressor of

ptc9 is a suppressor of lethal phenotype of oro1

Phenotype Manifest In
Enhanced by
NOT suppressed by

ptc9 has denticle belt | embryonic stage phenotype, non-suppressible by ihogKG/ihogKG

Enhancer of
NOT Enhancer of

ptc9/ptc[+] is a non-enhancer of wing phenotype of MoeC858

Suppressor of

ptc9 is a suppressor of phenotype of Bunspecified

ptc9 is a suppressor of phenotype of hhts2

NOT Suppressor of

ptc9/ptc[+] is a non-suppressor of wing phenotype of MoeC858

Additional Comments
Genetic Interactions

The wing defects seen in Moec858 homozygotes are unnaffected by ptc9/+.

Embryos with maternal/zygotic iHogKG and zygotic ptc9 show the denticle belt duplication phenotype of ptc9 single mutants and not the denticle belt fusion phenotype of iHogKG maternal/zygotic single mutants.

Stage 15 ptc9 wgl-17 double mutant embryos have the same number of genital disc precursor cells as wgl-17 single mutants. This is a reduction compared to wild type, and a huge reduction compared to ptc9 single mutant embryos. In contrast, stage 15 enE ptc9 embryos have increased levels of genital disc precursor cells, similar to levels seen in ptc9 single mutants.

mid1 ptc9 larvae show complete loss of denticle belts in odd-numbered segments.

The phenotype of Alg3tid1 ptc9 double mutant embryos resembles that of ptc9 single mutants.

In ptc9 ; ci94 double mutant embryos, naked cuticle is present but is more limited than in ptc9 single mutant embryos. This double mutant cuticle phenotype is "intermediate", resembling neither single mutant. Some segments are fused, and thoracic segments do not produce any naked cuticle. Abdominal denticle diversity is restored. Expansion of denticle types 2 and 3 is seen and type 4 and 5 denticles are seen laterally. The ectopic groove seen in ptc9 single mutant segments is not seen in the double mutant embryos.

ptc9 enE invE triple mutants lack RP2 neurons.

ptc9 oro1 double homozygous embryos have the same phenotype as ptc9 single mutant embryos, indicating that ptc is epistatic to oro. 96% of oro1 ptc9/oro1 + flies are viable. 46% of oro1 ptc9/Df(2L)al flies are viable. 81% of oro1 ptc9/oro2 flies are viable. smo1 ptc9 double homozygous embryos have a fused denticle belt phenotype, indicating that smo is epistatic to ptc. The eyes of ptc9/+ ; hhbar3/hhbar3 and ptc9/oro1; hhbar3/hhbar3 flies are similar in size, suggesting that ptc is epistatic to oro with respect to effects on hhbar3.

ptc9, wgl-17 double mutants have lateral whirls of denticles. In hh21;ptc9 double mutants the posterior cuticle within each segment is rescued. Characteristic posterior row of denticles is absent. Denticle belts appear broader and mirror image symmetry is not found. In ptc9, gsb- double mutants large posterior denticle of each abdominal belt are missing, region ventral naked cuticle is missing. Denticles of intermediate size pointing posteriorly cover the whole of the segments.

Xenogenetic Interactions
Complementation and Rescue Data
Rescued by
Partially rescued by

ptc9 is partially rescued by ptchs.PSa


ptchs.PSa construct can rescue the variable phenotype in combination with ptctuf-1 ptchs.PSa construct partially rescues the lethality and wing and wing venation defects seen in combination with ptcG20.

Images (0)
Stocks (2)
Notes on Origin

The expression of l(1)sc is unaltered in early homozygous mutant embryos.

gsb-n protein expression has been studied in ptc9 embryos.

Cuticle phenotype can be restored to wild type by P{HS-ptc}.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (86)