col, collier, collier/knot, knotted
Gene model reviewed during 5.44
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.50
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\kn using the Feature Mapper tool.
Comment: reported as dorsal/lateral sensory complexes
Comment: anterior compartment
kn is expressed in two regions of the wing disc, a region of the wing hinge primordium in the posterior compartment and a stripe in the A region that abuts the anterior/posterior compartment boundary.
Transcript is detected in 7 cells anterior to the A/P boundary in third instar wing discs. However, expression is excluded from the D/V boundary that will form the wing margin.
kn transcripts are expressed in the anterior-most regions of the mandibular segment and also in the cephalic mesoderm.
In late embryonic stage 12, kn is only detected in one founder cell per hemisegment, the dorsal acute muscle 3 (DA3) founder cell. At stage 13, during the process of myoblast recruitment by the founder cell and as fusion proceeds, kn is activated in the nucleus of each newly incorporated myoblast. At stage 14, all nuclei incorporated in the DA3 syncytium actively transcribe kn.
kn is expressed in a promuscular cluster and the three derived precursor cells at the origin of dorsal-lateral muscles. Specifically, kn is expressed in the dorsal acute muscle 3 and dorsal oblique muscle 5 (DA3/DO5) precursor, the ventral lateral longitudinal muscle 1 and dorsal oblique muscle (LL1/DO4) precursor, and the dorsal transverse muscle and dorsal oblique muscle 3 (DT1/DO3) precursor. These muscle precursor cells are first observable at different times during embryonic stage 11.
kn expression is first detected in the ventral nerved cord at embryonic stage 12 in about 20 cells per hemisegment. This increases to about 50 cells per hemisegment at stage 14 and later. These are mainly (stage 12) and only (stage 14) postmitotic cells and are neurons and not glial cells.
kn protein is localized in a segmentally repeated pattern in the somatic mesoderm, in cell clusters in the same dorsal position in all trunk segments. At stage 11, those cell clusters have given rise to the muscle founder cells that will become the DA3/DO5 and DO4/DT1 progenitors, and continue to express kn protein. After asymmetric division of the muscle founder cells, kn expression is maintained only in the fusion competent cell corresponding to the DA3 muscle, then in the DA3 muscle.
kn is expressed in the NB5-6 lineage in thoracic and abdominal segments and in some more anterior segments in a late temporal window.
kn is expressed in class IV multidendritic neurons, specifically the vdaB, vdaa, and ddaC ventral multidendritic neurons and also in dorsal acute muscle 3 (DA3) somatic muscles in stage 15 embryos.
kn protein is first detected during embryonic development of the lymph gland at emrbyonic stage 11, in two separate clusters of cells in the dorsal-most mesoderm of thoracic segments T2 and T3. These clusters converge and coalesce by early stage 13, forming the lymph gland primordium. During stage 14, expression is progressively restricted to posterior-most cells of the developing lymph gland; at late embryonic stages, kn protein expression marks the posterior signalling center of the lymph gland.
Protein is detected in 7 cells anterior to the A/P boundary in third instar wing discs. However, expression is excluded from the D/V boundary that will form the wing margin.
Expression in mesodermal cells in segments T3, A1, and A2 is shown. At embryonic stage 10, kn is expressed in one and two clusters of mesodermal cells in T3 and A1-A2. At stage 11 kn expression is restricted to the muscle precursor cells (one in T3, two in A1,A2) singled out from each kn-positive premuscular cluster. By stage 12, kn is expressed in two founder cells resulting from the division of each progenitor. At stage 13, kn protein remains in two (T3) or four (A1,A2) muscle precursors. At stage 14, kn is only detected in the dorsal acute muscle 3 precursor.
GBrowse - Visual display of RNA-Seq signalsView Dmel\kn in GBrowse 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.
Ectopic expression of kn increases arbor length and represses filopodia/spike formation in class III neurons.
kn is required for the proper positioning of veins 3 and 4 in the wing and to prevent ectopic venation between them.
kn is required for the formation of the hypopharyngeal lobe and for subsequent differentiation of the ventral arms and lateralgrate of the pharyngeal head skeleton.
kn shows lineage-specific restriction of transcription to the founder of muscle DA3A during muscle development, which depends on the asymmetric segregation of numb gene product and involves repression by N signalling.
The specification of the DA3A muscle lineage requires both kn and at least one other transcription factor.
kn is required for the establishment of the PS(-1)/PS0 parasegmental border and formation of the intercalary segment.
kn has a specific role in hh-mediated patterning of the wing with no appreciable effect on general dpp-mediated wing organisation. kn acts in the hh-responsive cells at the posterior edge of the anterior compartment of the wing, primarily by preventing vein formation by these cells, thus forming a distinct intervein region between veins 3 and 4.
Mutants display hyperplastic phenotype, showing tissue overgrowth in mitotic recombination clones.
Nichols-Skoog, 1st Aug. 1931.