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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.47
4.1 (northern blot)
4.3, 3.2 (northern blot)
469 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ap using the Feature Mapper tool.
Comment: reported as rectum specific anlage
ap transcripts are expressed in a subset of cells within the embryonic brain and ventral nerve cord, in a subset of embryonic muscles, and in wing discs. Within the ventral nerve cord, expression is restricted to 3 cells per hemisegment (one dorsal and two ventral) and an additional cluster of 4 lateral cells in each thoracic hemisegment.
ap transcripts are first detected on northern blots in 3-6hr embryos, peak in 9-12hr embryos and are expressed at lower levels in late embryonic and larval stages. ap transcripts are first detected by in situ hybridization in a segmentally repeated group of 16-18 cells. By 8hr, ap is expressed in several discrete clusters as a result of cell migration. The cells appear to be predominantly mesodermal and are occur in positions where ventral and mediolateral muscle precursors arise. Some of the cells are more closely associated with the ectoderm. In the CNS, ap is expressed in 5 postmitotic neurons per hemisegment in A1-A7 and an extra 4 neurons in the thoracic segments. 7 of the 9 ap-expressing neurons are found in positions where motoneurons that exit the CNS through the segmental nerve are found. ap is also expressed in the brain.
ap transcripts are expressed in a complex and dynamic pattern during embryogenesis. During germband extension, expression is observed in the mandibular lobe and in the anus. Later, ap expression is observed in PNS cells that are thought to be accessory cells associated with a subset of both chordotonal and external sensory organs. ap expression is also observed in other thoracic cells that may be larval muscle precursors. Finally, a restricted set of cells (1-4 per hemisegment) in the CNS express ap. ap expression is later observed in larval and pupal imaginal discs. Transcripts are expressed throughout the parts of the of the wing and haltere discs that give rise to the dorsal surface of the wing and haltere blades, at lower levels in the regions that form the notum and scutellum, and at the highest level in the wing hinge region. It is also expressed in the presumptive fourth tarsal segment of the ventral thoracic discs, in a central spot in the antennal portion of the eye antennal disc, and in the larval brain.
ap transcripts are expressed in a complex and dynamic pattern during embryogenesis. During germband extension, expression is observed in the mandibular lobe and in the anus. Later, ap expression is observed in PNS cells that are thought to be accessory cells associated with a subset of both chordotonal and external sensory organs. ap expression is also observed in other thoracic cells that may be larval muscle precursors. Finally, a restricted set of cells (1-4 per hemisegment) in the CNS express ap. ap expression is later observed in larval and pupal imaginal discs. Transcripts are expressed throughout the parts of the of the wing and haltere discs that give rise to the dorsal surface of the wing and haltere blades, at lower levels in the regions that form the notum and scutellum, and at the highest level in the wing hinge region. It is also expressed in the presumptive fourth tarsal segment of the ventral thoracic discs, in a central spot in the antennal portion of the eye antennal disc, and in the larval brain. ! GAT13b. Alleles or genotypes used :
Within the ventral nerve cord, expression is restricted to 3 cells per hemisegment (one dorsal and two ventral) and an additional cluster of 4 lateral cells in each thoracic hemisegment. Analysis of expression of a ap promoter fragment fused to tau-lacZ (see btauap.C.T:lacZ) suggests that the ap-expressing cells are interneurons.
Comment: expressions starts 36 hr APF
GBrowse - Visual display of RNA-Seq signals
View Dmel\ap in GBrowse 22-55
2-55.7
2-54
2-55.4
2-55.2
2-[55.2]
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: ap CG8376
Source for merge of: ap neuro
Identification: as a complementation group whose members dominantly modify the small wing phenotype caused by expression of Pi3K92ED954A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096. 4 alleles of ap have been recovered.
An enhancer element, apME680, is responsible for expression in muscle progenitors.
Shows particularly robust cycling of transcription in adult heads, as assessed by expression analysis using high density oligonucleotide arrays with probe generated during three 12-point time course experiments over the course of 6 days.
ap mediates development of direct flight muscles autonomously and development of indirect flight muscles through epidermal cues.
ap is not required for Tv neuron survival or morphological differentiation in the central nervous system, but helps define neurotransmitter expression in these neurons.
Genetic combinations with mutants of nub cause additive phenotypes.
Expression pattern analysis suggests a conservation of the tissue-specific gene networks operating in the muscles and neural tubes of flies and mice.
Tissue specific and homeotic regulation of ap are regulated through the same cis-acting sequences. Expression of the homologue during mouse embryogenesis suggests that aspects of its regulation and function have been conserved from Drosophila to mammals.
All ap-expressing neurons are interneurons that chose a single pathway within the developing central nervous system.
ap lethality is polyphasic, but occurs primarily at the larval and pupal stages. The lethal phenotype is not associated with any overt morphological abnormality, suggesting that death occurs from a systemic malfunction.
Clonal analysis suggests that short range interactions between ap expressing (dorsal identity) and non-expressing (ventral identity) cells induces the formation of the wing margin.
Spatially localized expression of apterous specifies the identity of dorsal cells in the wing.
Whereas in wild type ovarian follicles the Golgi apparatus and yolk spheres are preferentially labelled by osmium zinc iodide, in mutant follicles the Golgi apparatus and nearby vesicles showed dramatically reduced staining.
Though ap is expressed in the dorsal cells of the developing wing, it is required for formation of the entire wing.
Most of the characterized ap alleles belong to the group showing the ap1 or ap4 phenotype. Some alleles (apblt2 and apT60) have a less severe wing phenotype, being straplike. Alleles also vary in their expressivity of the precocious adult death and nonvitellogenic ovary phenotypic characters; some alleles result in a low number of escapers, similar to ap4, while others have an escaper percentage of as much as 50%. There is little correlation between expressivity of the wing deficiency phenotype and either precocious adult death or nonvitellogenic ovary development. Generally, heterozygous combinations of these alleles do not show complementation for any phenotypic characters. Another group includes two dominant alleles. The ap locus appears to be a complex locus, containing several partially complementing groups for the wing deficiency and adult-death/female-sterility phenotypic characteristics.
The ap locus is essential for the development of normal levels of male courtship and male mating success and for the loss of immature male sex appeal.
Abnormally low levels of juvenile hormone are synthesized in ap mutants.
The neuro gene product is likely to act as a transcription factor controlling the expression of genes involved in terminal differentiation of the subset of neurons and muscles that express it.
ap is essential for the normal acquisition of female receptivity to males.
Mutations at the ap locus alone cannot reduce female receptivity to males to zero. Juvenile hormone deficiency is the cause of low receptivity in mutants.
The ap locus is involved in male courtship.
All phenotypes of ap alleles are explicable in terms of changes in quantity rather than quality of gene product.
A good correlation exists between expressivity of the precocious adult death or nonvitellogenic ovary development phenotypes.