Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.50
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\abo using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\abo 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: abo CG6093
The insertion of the blood transposon in region 32E causes the pleiotropic abo mutant phenotype.
Progeny survival from abo mothers depends in part upon the maternal dosage of ABO-X heterochromatin: recovery of daughters decreased if the mother was ABO-X-/ABO-X- and increased if they received an ABO-X- X chromosome from a heterozygote mother. These results suggest an interactive effect between the ABO-X deficient X and the ABO-X heterochromatin in the maternal genome. The ABO-X heterochromatin on the X chromosome rescues zygotes from the abo maternal effect prior to the completion of the first zygotic division.
Maintained homozygous abo stocks show a decrease in maternally-induced embryonic lethality over time. The altered genetic factors responsible are abo-responsive heterochromatic rescuing regions that act zygotically, dominantly and additively to reduce lethality. The regions map to the second and X chromosome in the maintained homozygous abo stock.
Embryos, especially male, from females homozygous for abo mutant alleles have a reduced probability of survival, dying both before and after blastoderm formation. Postblastoderm lethality can be partially rescued by a paternal wild-type allele and preblastoderm lethality by the maternal effect of heterochromatic elements on the X, Y and 2R (defined as ABO-X, ABO-YL, ABO-YS and ABO-2R).