Disease relevance of cno

• Finally, we discuss the possibility that mis-regulation of post-transcriptional events can occur in certain neuromuscular diseases and cause abnormalities of the neuromuscular junction [1].
• Using polymerase chain reaction-single strand conformation polymorphism as an initial screening method, we identified one non-sense mutation, two mis-sense mutations and three silent mutations in five squamous cell carcinoma samples [2].
• The three squamous cell carcinoma samples containing non-sense and mis-sense mutations were isolated from individuals with histories of multiple basal cell carcinoma [2].

High impact information on cno

• Conversely, mis-targeting of oskar RNA to the anterior of the oocyte causes formation of ectopic abdomen and germ cells at the anterior pole [3].
• canoe encodes a novel protein containing a GLGF/DHR motif and functions with Notch and scabrous in common developmental pathways in Drosophila [4].
• This mis-expression of dpp could be correlated with some of the features of the adult mutant phenotypes [5].
• Incorrectly specified or mis-specified cells often undergo cell death or are transformed to adopt a different cell fate during development [6].
• In hid bicoid double mutants, mis-specified cells in the presumptive head and thorax survive and continue to develop, but they are transformed to adopt a different cell fate [6].

Biological context of cno

• Cno binds to the activated form of Rap1 in a yeast two-hybrid assay, the two molecules colocalize to the adherens junction, and they display very similar phenotypes in embryonic dorsal closure (DC), a process that relies on the elongation and migration of epithelial cell sheets [7].
• Direct binding between two PDZ domain proteins Canoe and ZO-1 and their roles in regulation of the jun N-terminal kinase pathway in Drosophila morphogenesis [8].
• Egfr signaling regulates ommatidial rotation and cell motility in the Drosophila eye via MAPK/Pnt signaling and the Ras effector Canoe/AF6 [9].
• Although mitosis is inhibited in the mis-expression animals, cells with abnormally large nuclei form tumor-like structures from continued endoreplication, cell growth and retinal differentiation [10].
• Targeted mis-expression of rap/fzr in the eye primordial cells causes precocious cell cycle exit, and smaller primordial eye fields, which either eliminate or drastically reduce the size of the adult eye [10].

Anatomical context of cno

• Immunolabeling of the Canoe protein in the pupal retinae showed that it was accumulated in adherens junctions in photoreceptor rhabdomeres at high concentrations, as well as in pigment cells, bristle cells, and the interjunctional region of photoreceptors at a lower level [11].
• Since Canoe or its mammalian homolog AF-6 is known to bind to F-actin and Ras, we suggest the possibility that Canoe couples Ras signaling with cytoskeleton, thereby supporting the straight elongation of rhabdomeres required for development of a regular array of ommatidia [11].
• Furthermore, expression of a green fluorescent protein (GFP):nanos 3'UTR fusion protein in germ cells shows that PGC migration is aberrant, and the mis-migrating PGCs do not survive in Stau-compromised embryos [12].
• The commissural defects seen in vnd gain-of-function mutants correlate with midline glial defects, whereas the mislocalization of interneurons coincides with longitudinal glial mis-specification [13].
• STAT92E-GFP fluorescence is increased in response to ectopic upd in the larval eye disc and mis-expression of the JAK kinase hopscotch in the adult fat body [14].

Associations of cno with chemical compounds

• Moreover, we show that fly viability and growth depend on the exquisite ratio between dNK expression and its substrate thymidine (dT) in the medium, and that increased dT concentrations trigger apoptosis and a decrease in body mass when dNK is mis-expressed [15].

Other interactions of cno

• Echinoid also links to actin filaments by binding to Canoe/AF-6/afadin [16].
• Genetic interaction experiments show that Rap1 and Cno act in the same molecular pathway during DC and that the function of both molecules in DC depends on their ability to interact [7].
• Our data indicate that, beside the Raf/MAPK cascade, the Ras effector Canoe/AF6 acts downstream of Egfr/Ras and provides a link from Egfr to cytoskeletal elements in this developmentally regulated cell motility process [9].
• We further show that regulatory Dl mutations or mis-expression of DL abolish leg segmentation [17].
• We found no genetic evidence to support a role for either Canoe or Armadillo in the essential Fat facets pathways in Drosophila eye development [18].

References