Updated sequence information for this Drosophila species is no longer provided by FlyBase. Gene model annotations for this species are now updated and maintained at NCBI, using the gnomon automated annotation pipeline. See the NCBI page ‘Eukaryotic genomes annotated at NCBI’.
The FlyBase BLAST tool will continue to support queries against the reference genome of this species, but not queries against annotated transcripts or proteins. For the current release, there is no JBrowse or GBrowse view of the gene model annotations for this species.
The FlyBase archived release FB2017_05 includes the last NCBI annotation update for this species that was imported into FlyBase. That sequence data can be accessed from archived gene reports, via the archived GBrowse tool, and via archived bulk-data downloads.
Hmr
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.
Upregulation of transposable element transcription is seen in hybrids between D. melanogaster and D. simulans, but this is unlikely to be the direct cause of hybrid lethality.
The Hmr and Lhr proteins form a centromeric complex in D. melanogaster which is required for proper chromosome segregation during mitosis. Both an increase and a decrease in complex levels result in mitotic defects, indicating that this function is extremely dose sensitive. Alteration of the levels of the complex also result in an increase in transcription from transposable elements.
The level of Hmr expression in D melanogaster is substantially higher than the expression of the orthologous Dsim\Hmr gene in D. simulans. Conversely, the expression of the D. simulans Dsim\Lhr gene is higher than the expression of the orthologous Lhr gene in D. melanogaster. Hybrids derived from a cross between D. melanogaster females and D. simulans males thus have an elevated amount of the Hmr-Lhr protein complex compared to the parent species, and the complex is delocalised, being bound to numerous interbands along all chromosome arms in the hybrids. Hybrid males and females show a massive increase in transcription from transposable elements, but as the effect is not sex-specific, this is presumably not the the main cause of the lethality of hybrid males.
A Dsim\Hmr+ transgene has no phenotypic effect in D.melanogaster/D.simulans and D.melanogaster/D.mauritiana hybrids and a Dmau\Hmr+ transgene has no phenotypic effect in D.melanogaster/D.simulans and D.melanogaster/D.mauritiana hybrids, strongly supporting the conclusion that the Hmr gene has functionally diverged between the D.melanogaster and sibling-species (D.simulans and D.mauritiana) lineages, to cause F1 hybrid incompatibility between these species. Phylogenetic analysis shows that Hmr has diverged extensively in the D.melanogaster lineage, but extensive divergence has also been found in the sibling-species lineage. Together, the findings implicate over 13% of the amino acids encoded by Hmr as candidates for causing hybrid incompatibility. The exceptional level of divergence at Hmr cannot be explained by neutral processes, as phylogenetic methods and population genetic analyses show that the elevated amino-acid divergence in both lineages is due to positive selection in the distant past - at least one million generations ago.
