Cos2, Costal2, cos-2, Costal-2, Costal 2
Gene model reviewed during 5.48
1201 (aa); 175 (kD observed); 133 (kD predicted)
Polyubiquitinated by Ubr3, which leads to proteasomal degradation.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\cos using the Feature Mapper tool.
In syncytial embryos, cos protein is distributed uniformly in the cortical cytoplasm. In the late syncytial embryo, it accumulates between and apical to nuclei. From the surface, the pattern looks like a honeycomb. Throughout cellularization, cos protein is associated with furrow canals and during late cellularization is associated with expanded furrow canals. In cellular blastoderm embryos and during gastrulation, cos protein is in the cytoplasm and at the periphery of all cells. A striped pattern of cos protein is observed beginning in late stage 9 and decaying in stage 12. Each stripe is continuous along the dorsal/ventral axis both in the ectoderm and the underlying mesoderm. The stripes appear to form in the anterior compartment of each segment. In wing discs, cos protein levels are elevated in the anterior compartment
GBrowse - Visual display of RNA-Seq signalsView Dmel\cos in GBrowse 2
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.
Source for identity of: cos CG1708
Identified as a component of the hh signalling pathway in a genome-wide RNAi screen. dsRNA made from templates generated with primers directed affects the extent of expression of a hh signaling reporter construct in Clone 8 cells.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
dsRNA made from templates generated with primers against this gene tested in an RNAi assay in S2 cells.
Epistatic analysis places cos function downstream of ptc and smo.
The last 301 amino acids of the cos COOH terminus are sufficient to provide full association with smo.
1 allele of cos been recovered in a screen for mutations with mutant phenotypes in clones in the wing.
Mutants are isolated in a screen of the second chromosome isolating disc morphology defects.
hh elicits signal transduction via a complex that includes the products of the fu, ci and cos genes. The complex binds with high affinity to microtubules in the absence of hh protein, but not when hh is present. The complex may facilitate signalling from hh by governing access of the ci product to the nucleus.
cos encodes a kinesin-related protein that accumulates preferentially in cells capable of responding to hh signal. The product is cytoplasmic and binds microtubules. The ci protein associates with the cos product in a large protein complex, suggesting that cos directly controls the activity of ci.
cos function is required maternally for the patterning of the central portion of each segment, in the absence of cos activity the central portion is replaced by a mirror image duplication of the anterior partion. The cos protein may be involved in localisation or transport of other segment polarity gene products within the cell, facilitating cell polarisation.
Mutants display hyperplastic phenotype, imaginal disc overgrowth.
Genetic and developmental characteristics of the imaginal disc overgrowth mutant have been determined.
cos suppresses the segment polarity and zygotic phenotype of one class of fu alleles and causes a lethal interaction with the other class of fu alleles.
cos falls into the segment polarity class of genes, and has both a maternal and a zygotic action.
Leaky alleles of cos display wing duplications that are part of a larger syndrome of polarity defects that affect the embryonic and imaginal segment. The dominant phenotype seen in flies heterozygous for the neomorphic "Cos" mutants is the result of a reduced level of function at the cos locus. Haploidy for cos enhances, whereas triploidy for cos suppresses the phenotype of "Cos" heterozygotes.
Homozygotes, hemizygotes and heteroallelic heterozygotes for class I alleles die as embryos with a normal cuticular phenotype. When derived from homozygous ovarian clones, however, abnormal deletion-duplication patterns in each segment are observed; posterior rows of abdominal denticles are replaced by mirror-image duplications of the anterior rows, including the segmental boundary, which is thereby duplicated; thoracic denticle belts missing; cos1 especially severely affected in this regard, including loss of entire segments. Heterozygotes derived from homozygous ovarian clones show slightly abnormal segmental patterning. Flies heterozygous for class I alleles or cos deficiencies and at the same time heterozygous for Cos alleles display pattern duplications of wings and halteres. Class II alleles are hemizygous lethal but homozygous viable. They display wing and haltere duplications indistinguishable from those found for cos1/Pka-C1Cos-1 heterozygotes as described by Whittle. Flies heterozygous for class III alleles and Cos show moderately reduced viability and occasional wing duplications; flies homozygous for class III alleles show reduced viability and have wild-type phenotype, but enhance the pattern duplications associated with Cos/+; hemizygotes for class III alleles or heterozygotes with class I alleles are lethal or nearly so in the presence of Cos, the survivors invariably exhibiting pattern duplications of wings and halteres.