Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.45
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\dop using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\dop 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: dop CG6498
"dop" is not allelic to "AGO2".
In contrast to what is stated in FBrf0194224, the "drop out" complementation group is not allelic to "AGO2". Recently isolated mRNA null mutations of the AGO2 locus fully complement dop mutant alleles. The molecular lesions of dop mutant alleles were reported in FBrf0194224 to represent in frame deletions of glutamine rich repeats (GRR) in the amino-terminus of AGO2. Analysis of 24 different D.melanogaster haplotypes show that the amino-terminal domain of AGO2 is highly variable and that the alteration of the amino-terminal GRR pattern observed in the dop allele is not unique. The GRR haplotype of dop is not the cause of the developmental phenotype of embryos derived from homozygous mothers. A D.melanogaster strain with the identical GRR haplotype does not exhibit gross developmental defects.
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, an increase in the proportion of G2/M phase cells and chromosome alignment defects are seen.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.