|Feature type||allele||Associated gene||Dmel\cora|
|Also Known As||cor5|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
Homozygous cora5 mutants and corak08713/cora5 transheterozygotes show electrophysiologically detectable loss of glutamate receptors.
The tracheal systems of lates stage cora5 homozygous embryos have overgrown tubes with unusual expansions, defects in the accumulation of lumen antigens and lumen breaks.
cora5/cora15 mutant wings exhibit a wing hair chevron phenotype and matches of non-parallel alignment.
In cora5 homozygous mutants the adherens junction remains intact, with the regular spacing of plasma membranes maintained. However, the septae normally located between these membranes are reduced in number or absent. cora5/cora5 somatic clones generated in larvae (approx. 72 hours after egg laying) do not survive in adult tissues.
In cora5/cora4 embryos, tracheal phenotypes are apparent from stage 15. At stage 16 in these embryos the average dorsal trunk length is significantly greater than wild type (P<0.005) (122+/-2% mean+/-s.e.m., n>5, normalized to stage 16 wild-type value). In addition these embryos have moderately severe diameter increases in the dorsal trunk and other primary tracheal branches, and some ganglionic branches exhibit missing lumen. Diameter increases are also seen in the primary tracheal branches of cora5 homozygous embryos. Unlike wild-type, post stage 15 trachea in cora5 homozygotes are unable to exclude from their lumens, a fluorescently labelled 10kDa dextran injected into the body cavity. This is consistent with these trachea lacking a functioning septate junction barrier.
Homozygous embryos have a dorsal open phenotype, cuticular thinning, necrosis of the salivary glands and a tracheal inflation defect. Embryos lack the individual septae that normally characterise the pleated septate junction. The salivary gland epithelium shows permeability to rhodamine-dextran, in contrast to wild type.
Homozygous embryos have a faint cuticle and a dorsal hole. The remains of the salivary glands are present as necrotic material. The epicuticle fails to adhere to the procuticle. The pleated septae that normally characterise the pleated septate junction are absent in mutant epithelia, and the transepithelial barrier function of the septate junction is also disrupted. The adherens junction appears unaffected in mutant embryos. No adult escapers are produced. Hemizygous embryos have a dorsal hole and detached cuticle. The denticle belts contain fewer denticles than normal, although the overall pattern of the denticle belts is normal.
Homozygous embryos have dorsal closure defects; dorsal holes are seen in the cuticle. Necrosis is seen in the salivary glands.
|Phenotype Manifest In|
|NOT Enhanced by|
|NOT suppressed by|
|NOT Enhancer of|
|NOT Suppressor of|
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
|Secondary FlyBase IDs|
|References ( 15 )|