tuf, rubr, Ptch
transmembrane protein - segment polarity gene - receptor for Hedgehog - The reception and transduction of the HH signal is mediated by its receptor Patched and by Smoothened - PTC and HH control SMO by regulating its stability, trafficking, and phosphorylation - SMO in turn interacts directly with Fused and Costal2, which interact with each other and with Cubitus interruptus in an intracellular Hedgehog transducing complex
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Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.49
6.3 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
1286 (aa); 143 (kD)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ptc using the Feature Mapper tool.
In the trunk ectoderm of stage 11 embryos, ptc expression is confined to two ectodermal stripes in each parasegment, one on either side of the hh stripe. In the visual primordium, ptc is present only in anterior optic lobe cells adjacent to the posterior optic lobe. ptc is also expressed in tracheal pits and most prominently in the anterior part of the pits.
Transcript is detected in 5 cell widths at the A/P boundary in third instar wing discs. However, expression is excluded from the D/V boundary that will form the wing margin.
In wghs.PN embryos, 3 hours after the last shock, the ptc domain becomes confined to those cells that do not express en. The anterior border of the ptc stripe coincides with the deep groove that marks the posterior limit of the broadened en stripe. This is a similar expression pattern to that found in nkd mutant embryos.
ptc transcripts are expressed predominantly in early embryos with lower levels in late embryos, larvae, and pupae. They are first detected at nuclear cycle 14 and are present throughout the cortical region of the embryo except for a dorsal anterior patch and a posterior patch including the pole cells. From gastrulation through mid-germband extension they are uniformly distributed. By the end of stage 8, a pattern of 15 stripes develops with expression also observed in the hindgut/analia and in the labrum. During the extended germ band stage, each broad stripe splits into two stripes. The cells in the middle of the original stripes no longer express ptc. Expression is also seen in various regions of the head, CNS, mesoderm, and around the incipient Malphigian tubules. The regions of expression in each segment were mapped to the anterior-most cells of every segment and the posterior cells of every parasegment.
ptc is found in a large number of axon tracts. It is present in the dendritic fibers of the mushroom body calyx and Kenyon cells but not in the rest of the mushroom body. It is also observed in nerve fibers of the antennal lobe, anntennal nerve bundle, and secondary projections of the retina and several other structures.
ptc protein is expressed at similar levels in wing and haltere discs.
Protein is detected in 5 cell widths at the A/P boundary in third instar wing discs. However, expression is excluded from the D/V boundary that will form the wing margin. margin.
Protein is detected in portions of the eye-antennal disc that will form the head capsule.
GBrowse - Visual display of RNA-Seq signals
View Dmel\ptc in GBrowse 22-57.8
Maps near Bl.
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Source for identity of: ptc CG2411
Source for merge of: ptc rubr
Source for merge of: ptc Conf
Source for merge of: ptc BcDNA:RH36596
Source for merge of ptc BcDNA:RH36596 was a shared cDNA ( date:030728 ).
ptc is required for proper tracheal ganglionic branch morphogenesis.
ptc is not required for tracheal ganglionic branch fate determination or the formation of tracheal cellular extensions.
Loss of ptc activity in the neuroectoderm prior to the formation of S1 and S2 neuroblasts causes the majority of axon guidance defects.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Epistatic analysis places cos function downstream of ptc and smo.
Two EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
ptc protein normally binds hh gene product without any help of the smo gene product, though smo is also a part of the receptor complex that binds hh and transduces the hh signal. The mechanism of signal transduction may involve hh binding specifically to ptc and inducing a conformational change leading to the release of latent smo activity.
Each primordia of the genital disc (female genital, male genital and anal primordia) is divided into anterior and posterior compartments. Clonal phenotype of genes known to play compartment specific functions demonstrate the anterior/posterior patterning functions of these genes are conserved in the genital disc.
Genetic combinations with mutants of nub cause additive phenotypes.
The pattern of expression of ptc in the larval and adult abdomen has been analysed.
ptc function is required for the formation of NB4-2 and specification of identity. ptc and gsb interact during specification of the NB4-2 identity, but not during delamination of NB4-2 from the neuroectoderm. ptc signalling pathway directly represses the gsb expression in row 4 neuroblasts and their precursor neuroectoderm.
Clonal analysis demonstrates that constitutive Mmus\Pkaca activity does not compensate for loss of ptc gene function.
hh pathway mutants induce ectopic morphogenetic furrows. Results show that ommatidial clusters are self-organising units whose polarity in one axis is determined by the direction of furrow progression and which can independently define the position of an equator without reference to the global coordinates of the eye disc.
Mutations in ptc show strong-non-autonomous effects in clones induced in the developing eye. Both ptc and Pka-C1 are required for the correct regulation of morphogenetic furrow progression, apparently via repression of dpp. Loss of function of either ptc or Pka-C1 in cells anterior to the furrow results in an ectopic furrow characterised by non-autonomous propagation of dpp expression outside the mutant tissue and ectopic photoreceptor differentiation. Both ptc and Pka-C1 act downstream of hh.
Viable mutations in the segmentation genes ptc cause specific alterations in dpp expression within the anterior-posterior compartment boundary of the wing disc. ptc gene product controls dpp expression in the imaginal discs and the restricted expression of dpp near the anterior-posterior compartment boundary is essential to maintain the wild type morphology of the wing disc.
Wild type activity of five segment polarity genes, wg, ptc, en, nkd and hh, can account for most of the ventral pattern elements in the embryo. wg is required for naked cuticle and en is required for the first row of denticles in each abdominal denticle belt. Remaining cell types are produced by different combinations of the five gene activities. wg generates the diversity of cell types within the segment but each specific cell identity depends on the activity of ptc, en, nkd and hh. ptc and nkd may affect wg autoregulation, and restrict wg activity within the segment. ptc and hh show mutual suppression through opposing effects on wg expression.
Transcriptional control of both ptc and wg by hh is mediated by the same signal transduction pathway. Transcriptional control of ptc is mediated by fu and ci. fu and ci are required for normal wg transcription, acting downstream of ptc to regulate wg transcription. cos negatively regulates ptc and wg transcription. Ecol\lacZ reporter gene constructs demonstrate cis-acting control elements drive ptc expression specifically in cells flanking the hh domain.
Segment polarity mutations cause stripes of abnormal patterning within sectors of the leg disc, which may be mediated by regional perturbations in growth.
The ptc and hh genes encode components of a signal transduction pathway that regulate the expression of wg transcription following its activation by pair rule genes, but most other aspects of wg expression are independent of ptc and hh. The suppression of ectopic wg transcription in pair rule mutants depends on ptc. Expression of wg in the absence of ptc depends on hh. Absence of ptc activity can result in de novo activation of wg after gastrulation.
The pattern of ptc protein expression during embryonic development has been analysed.
Dfd expression unaffected by mutations at this locus.
Expression of hh in patch mutants analysed.
Ectopic uniform wg expression results in patched being expressed in those cells that are not expressing en (as in wild type), but since the en stripe is broader the patch stripe is thinner.
Pattern of hh expression in ptc mutants studied. In the absence of ptc function, wg expression, which is normally en-dependent, no longer requires en.
The ptc phenotype cannot be completely rescued when in double mutant combination with wg, hh, en or gsb. This suggests that ptc is specifically required for patterning of the central cells of each segment.
The role of ptc in positional signalling is permissive rather than instructive, its activity is required to suppress wg transcription in cells predisposed to express wg. These cells receive an extrinsic signal, encoded by hh, that antagonises the repressive activity of ptc. Results suggest that ptc protein may be the receptor for the hh signal, implying that this is an unusual mechanism of ligand-dependent receptor inactivation.
Mutations in zygotic polarity gene patch do not interact with RpII140wimp.
nkd and tuf mutant embryos show ectopic expression of Ba in the limb primordia. There is a correspondence between the Ba expression and the spatial organization of the larval and adult limbs that develop from the primordium.
ptc is negatively regulated by en in the early extended germ band. ptc parasegmental boundaries are shifted in nkd embryos forming posterior to each en domain: expression domain is reduced. After stage 11 most ptc transcripts begin to disappear and by the end of germ band retraction ptc is absent from most of the cells in wgl-17, hh21 and en- embryos. Late ptc transcription patterns depend upon selective repression by ciD and itself.
The role of ptc in patterning the cuticle of the adult fly has been analysed.
The role of segment polarity genes in arm protein accumulation has been investigated.
The ptc gene encodes an integral membrane protein with multiple membrane spanning domains.
ptc has a specific role in the control of cell fates during neurogenesis: ptc specifies a subset of neuroblasts and neural progeny.
The ability of ptc mutant embryos to produce adult structures when cultured in vivo has been analysed.
The ptc gene is involved in patterning within segments in Drosophila. The viable first-identified mutant has a small tuft of hairs between eyes and antennae and shows basal twinning of the anterior halves of wings; it overlaps wild type. ptc/Tp(2;3)dp has an extreme form of this mutant phenotype. Other mutants are embryonic lethals of the segment-polarity type. There is a mirror-image duplication of segment boundaries and adjacent cuticle of all segments with deletion of the remainder of the segment. Defect visible during extended-germ-band stage (6 hr) (Nusslein-Volhard and Wieschaus, 1980). Normal number of denticle bands; duplicated region of embryo includes some naked cuticle anterior to denticle bands. Pattern of neurons underlying affected epidermal region is altered (Patel et al., 1989). This mutant has no effect on the spatial expression of the 'pair-rule' mutant ftz (Carroll and Scott, 1986). ptc embryos cultured in vivo produced derivatives of the eye-antennal and thoracic discs, the latter being abnormal in morphology and in en expression (Simcox et al., 1989).
