kek, kekkon, kek-1, kekon, uns
Ig domain protein, Leucine-rich repeat protein - plays a role in axonal outgrowth in the central nervous system - acts in a negative feedback loop to modulate the activity of the Egfr tyrosine kinase during oogenesis
880 (aa); 92 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\kek1 using the Feature Mapper tool.
Expression pattern inferred from unspecified enhancer trap line.
kek1 transcripts are detected in9-13hr embryos on northern blots. They are detected by in situhybridization early in the midline and later in most neurons in the CNS.In the PNS, they are expressed in cap cells and weakly in ventral andlateral clusters. They are also expressed in the antenno-maxillary complexand in ovaries in a pattern similar to that of the corresponding enhancertrap line (Ecol\lacZkek1-15A6).
GBrowse - Visual display of RNA-Seq signalsView Dmel\kek1 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 merge of: kek1 BEST:GM02380
The leucine rich repeats of kek1 protein are sufficient for binding Egfr protein, however, inhibition of Egfr protein by kek1 protein in vivo requires the kek1 juxta/transmembrane region. kek1 protein is not a phosphorylation substrate for the Egfr protein in vivo.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a phenotype when assayed in Kc167: binucleate cells.
Original 'unstrung' phenotype was in fact due to deletion of more than one gene, one of which has been shown to be kek1.
kek1 expression is regulated in the developing epithelia in addition to the CNS. The absence of kek1 gene product causes no overt phenotype. Results suggest kek1 and kek2, or additional genes, may overlap in function in the assembly of the CNS.