sple, pk-sple, prickle-spiny legs, prickle-spiny-legs
LIM domain protein - a tissue polarity protein - in the Dachsous-Fat system, Dachsous and Dachs, each independently interacts with the Spiny-legs isoform of Prickle and direct Spiny-legs localization in vivo
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
5.1, 4.2 (northern blot)
None of the polypeptides share 100% sequence identity.
1206, 936, 870 (aa)
Interacts with dsh; PET and LIM domains interact with dsh DEP domain, in wing cells. Interacts with Vang in photoreceptor cells.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\pk using the Feature Mapper tool.
In 28-34hr pupal wings, pk transcripts are expressed uniformly in intervein cells but not in presumptive vein regions. In pupal legs, transcripts are uniform in most cells but are excluded from the segmental boundaries. Low levels are detected in restricted domains in larval imaginal discs. In the eye disc, expression is detected in a stripe of cells behind the morphogenetic furrow. In wing discs, expression is higher along the dorsoventral compartment boundary. In embryos, a dynamic expression pattern is observed. Expression is highest in cells engaged in morphogenetic movements such as invaginating midline cells, the cephalic fold, and at parasegmental boundaries. Expression of the "pk" and "sple" isoforms is indistinguishable.
"pkM" transcripts are detected only in embryos.
pk protein is expressed in the cytoplasm of all sensory neurons and their axons and in the epidermis from embryonic stage 13 on through embryogenesis. It is also expressed in motor axons including motor nerve SNa in stage 16 embryos. High levels of pk are seen in the dendrites of chordotonal neurons at this stage.
GBrowse - Visual display of RNA-Seq signalsView Dmel\pk in GBrowse 2
Alleles of the 'prickle' phenotypic class map to the left of alleles of the 'sple' phenotypic class.
Genetic map position is approximate.
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.
During development of the bristle lineage, Vang protein is localised in an anterior crescent in dividing sensillum precursor cells.
in and fy are needed for cells to respond to pk and stan. Genetic analysis is not consistent with fz-like class of genes fz, pk, Vang, stan and dsh acting simply as positive or negative regulators of in and fy.
pk is required for a feedback loop that generates asymmetric planar cell polarity signalling in the wing.
The "Pk" class of alleles carry molecular lesions within the proximal 30kb of the transcription unit, whereas the "Pk-Sple" class of alleles map to the distal section of the transcription unit. In direction of increasing cytology: Spn43Aa+ pk+ Spn43Ab- nec- pk+ Ady43A-
Alleles can be divided into three phenotypic classes, "Pk", "Pk-Sple", and "Sple". No allele causes an embryonic phenotype, even when homozygous mutant embryos develop from homozygous mutant mothers. Deletions of the pk gene are fully viable and fertile. The defects of the double mutant "Pk-Sple" class are the same as those seen with deletions of the entire gene. Paradoxically the "Pk" and "Sple" classes give more severe phenotypes with "Pk" affecting the wing and notum and "Sple" in the legs abdomen and eyes.
The balance between the pk isoforms "Pk" and "Sple" is critical for the specification of planar polarity.
pk is a slightly haploinsufficient gene. A deficiency for pk (and some pk point mutants) shows a weak, partially penetrant dominant tissue polarity phenotype. This effect is enhanced by several Vang alleles. Phenotypic data suggest that genetics of Vang and its interactions with pk are complex. Several, but not all, Vang alleles act as enhancers of the pk haploinsufficient tissue polarity phenotype, and the pkTBJ21 antimorphic phenotype. Mutations in pk can also act as suppressors of Vang dominant phenotypes.
Mutants do not exhibit defects in the denticle belt of hairs of the larvae.
In pk mutants the dorsal/ventral boundary in the eye is respected but the mechanism for ommatidial polarization is perturbed. A likely explanation for the observed phenotype is that the fates of dorsal and ventral cells within a cluster have been interchanged.
Mosaic analysis demonstrates pk function in either R3, R4 or R5 photoreceptor cell appears to be sufficient to drive an ommatidium in the right direction.
Polarity pattern of wing, haltere and notum altered. Triple row bristles on anterior wing slanted proximally instead of distally. On the notum, the posterior acrostichal bristles are whorled.
Trichomes near L2 vein arranged in counterclockwise whorl on right wing blade, in clockwise whorl on left blade; trichomes in anterior wing occasionally duplicated. Somatic clones of homozygous pk mutant cells have been generated. Not a vital locus.
"AQ254872; BDGP:EP (2)2557" was stated as revision.
Ives, Nov. 1938.