Gene model reviewed during 5.51
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\Hmr using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Hmr in GBrowse 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 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: Hmr BcDNA:LD22117
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.
It is possible that "anon-AE003451.1" should be merged with " BcDNA:LD22117 " to make a single gene.
sesB and Ant2 do not correspond to Hmr; Hmr maps distal to both genes and neither sesB mutant alleles nor transformants carrying extra copies of sesB and Ant2 have any effect on interspecific viability.
Source for merge of Hmr BcDNA:LD22117 was sequence comparison ( date:030514 ).
The Hmr and Lhr proteins form a heterochromatic complex with Su(var)205 in D. melanogaster. Hmr and Lhr are required to repress transcripts from satellite DNAs and many families of transposable elements. They are also required to help regulate the length of telomeres (which in Drosophila are composed of domesticated transposable elements).
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 orthologous D. simulans Dsim\Hmr and Dsim\Lhr proteins also bind each other in coimmunoprecipitation experiments and also localise to the centromere (although Dsim\Hmr also shows a prominent non-centromeric localisation).
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.
Hmr is required for wild-type levels of viability and fertility of D.melanogaster females.
Mutations in the D.melanogaster gene Hmr, along with unidentified polymorphic factors, rescue the agametic phenotype of F1 hybrid females derived from crosses of D.melanogaster females to either D.simulans or D.mauritiana males. F1 hybrid males from these crosses are fully sterile. The F1 hybrid females produce small numbers of progeny in backcrosses to D.melanogaster males, the low fecundity being caused by incomplete rescue of oogenesis as well as zygotic lethality.
The wild-type product of Hmr is neither necessary nor sufficient for embryonic inviability in hybrids between D.melanogaster and its sibling species. Hmr does, however, appear to lower the viability of hybrid larvae. This data suggests that Hmr acts as a gain-of-function poison in hybrids.
Hybrid female progeny resulting from crossing D.simulans females to D.melanogaster males die as embryos. Hybrid males from the reciprocal cross die as late larvae, unless the male parent is mutant at Dsim\Lhr, or the female at Hmr. Hybrid males from D.simulans attached X females and D.melanogaster males are lethal at both embryonic and larval stages, but are rescued to viability by the Hmr mutant in the male parent and the Dsim\mhr mutant in the female parent.