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FB2026_01
,
released March 12, 2026
MAST205
Please see the JBrowse view of Dmel\dop for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
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.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
JBrowse - Visual display of RNA-Seq signals
View Dmel\dop in JBrowse3-43
3-37.2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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 JBrowse 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.
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.
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[46] allele is not unique. The GRR haplotype of dop[46] 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.
FlyBase curator comment: In contrast to what is stated in FBrf0194224, the "drop out" complementation group is not allelic to "AGO2" (see FBrf0211203 for more details).
