HMG-D, HMG D, HMG1
Apparent introns not annotated: probable artifacts due to repetitive sequence.
Gene model reviewed during 5.51
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.56
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\HmgD using the Feature Mapper tool.
HmgD transcripts are present throughout the germarium. They are also present in all of the germline nurse cells and the somatic follicle cells in stage 1-6 egg chambers. From stage 7, HmgD transcripts stop accumulating in the follicle cells but continue to be present in the nurse cells. They accumulate around the periphery of the oocyte and remain localized until the end of oogenesis. In early embryos, weak general expression is observed. HmgD expression resumes in stage 9 embryos where strong staining is seen in all neuroblasts. Starting in stage 11, staining is observed in a subset of cells of the PNS. Nervous system staining persists through most of embryogenesis. No staining is observed in commissures or longitudinal connectives.
HmgD transcripts are observed mainly in embryos and adult females on northern blots.
HmgD protein is present at a constant level throughout embryogenesis but the number of molecules per nucleus declines with each cleavage cycle.
GBrowse - Visual display of RNA-Seq signalsView Dmel\HmgD 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.
Candidate stable intronic sequence RNA (sisRNA) identified within 5'UTR of this gene.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of HmgD results in an almost complete block of primary dendrite extension and lateral branching of ddaD and ddaE neurons. RNAi also causes defects in muscle and defects in dendrite morphogenesis.
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
The strength and selectivity of DNA binding by the HmgD HMG domain is modulated by the C-terminal basic and acidic domains.
HmgD is an architecture specific protein that prefers to bind to deformable DNA sites, A/T rich DNA containing the readily deformable dinucleotide sequence TG. HmgD binds preferentially to pre-bent DNA sites and induces substantial bends in DNA.
Immunological studies reveal that HmgD, either by itself or in conjunction with other chromosomal proteins, induces a condensed state of chromatin that is distinct from and less compact than the His1 containing 30nm fibre and this chromatin could facilitate rapid nuclear cycles.
HmgD transcripts display a complex pattern of temporal and spatial localisation implying a specialised rather than general role during early development.