Gene model reviewed during 5.47
No extensive homology to other protein sequences in the databases was observed. The H protein is highly basic overall but has a >100 aa stretch that is very acidic surrounded by particularly basic regions. Long homopolymeric runs of alanine residues are also present,especially near the carboxy terminus.
One of a couple of products generated by alternative splicing.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\H using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\H 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 identity of: H CG5460
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
gro and H control different aspects of ato's complex expression pattern. H represses ato expression in territories far ahead of the morphogenetic furrow, while behind the morphogenetic furrow H ensures the timely selection of regularly spaced R8 precursors, presumably by modulating N signaling.
Subcellular localisation of H protein shows a major focus of activity within the nucleus.
Candidate gene for quantitative trait (QTL) locus determining bristle number.
H acts by inhibiting signal transduction rather than by promoting signal production, during both selection of microchaete precursors in the notum and vein cell differentiation in the wing. H plays no essential role during embryogenesis.
Definitive denticle belt phenotypes (abnormal hairs and/or bristles) are foreshadowed by abnormal organisation of the actin cytoskeleton in embryonic epidermal cells.
Mutations show strong interactions with high and low selection lines, abdominal and sternopleural bristle numbers are affected. Results suggest H is a candidate for bristle number quantitative trait loci (QTL) in natural populations or is in the same genetic pathway.
Glutathione-S-transferase (GST) fusion proteins and the yeast two hybrid system demonstrate the H protein can inhibit the in vitro DNA binding activity of Su(H) through direct protein-protein interactions. Co-transfection assays in S2 cells demonstrate transcriptional activation driven by Su(H) is also inhibited by H.
N receptor activity suppresses H function during adult external sense organ development. H activity insulates sensory organ precursor cells from inhibition by N. H function appears to be an integral negative regulatory element of the N signalling pathway.
Overexpression of a wild type construct causes premature lethality and gain of function phenotypes, at ambient temperature it still rescues the dominant loss of function phenotypes. Mutant derivatives have allowed separation of a lethally mutable domain from a neural domain required for sensory organ formation.
In vitro binding assays demonstrate the H gene product can inhibit the DNA binding of Su(H) through direct protein-protein interactions. Consistent with this, transcriptional activation driven by Su(H) in transfected S2 cells is inhibited by H. These results support a model in which H acts, in part, as a negative regulator of Su(H) activity.
Dominant lethal interaction of an allele of H with kniri-92f reported: transheterozygotes are never recovered.
The H gene product is involved in the early nervous system differentiation and counteracts the action of other neurogenic genes.
NM1 defines a new class of Notch allele: similarity with and lack of specificity of interaction of N- and NM1 with H, mam, gro and E(spl) suggest that the NM1 effect is due to modification in the intracellular signalling of the activated N receptor.
Whereas H mutant alleles cause trichogen to tormogen double socket phenotype, heat shock ectopic Hairless-expression experiments produce double shaft tormogen to trichogen transformation, and bristle multiplication/loss phenotype similar to those caused by loss of function Notch mutations. Sensory organ precursor cell fate may require H to antagonise neurogenic gene functions and expression of distinct trichogen/tormogen sister cell pair may depend on asymmetry of H+ activity or their response to it. H has been cloned beginning with plasmid rescue of the insertion in HD179. Heat shock driven H+ line has been generated that rescues mutant H alleles. Mutant phenotype and expression studies suggest that neither fine spatial/temporal regulation nor high levels of H transcription are required for normal H function.
In H mutants, neuronal precursors do not differentiate: H may be involved in specifying neuronal cell fate. H mutations show genetic interactions with neurogenic mutations.
Genetic and molecular study of H function reveals that H is one of a small number of genes for which the loss of function phenotype is the failure of sensillum precursor development.
Lack-of-function alleles of H correct ASC "Hw" phenotypes in both ectopic and normal positions.
H is an enhancer of spl alleles of N: due to the haploinsufficiency of the H locus.
Mutations in H cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.
H dominantly suppresses the dx adult wing and ocelli phenotypes. Flies heterozygous for H and homozygous for dxENU have eyes smaller than wild type, infrequent missing or duplicated bristle phenotype and ommatidia are square wih a bristle at each corner.
ve, vn, ci, cg, svs, ast, H, Vno and vvl belong to the vein phenotypic group (Puro, 1982, Droso. Info. Serv. 58:205--208 ) within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutations within members of this group remove all veins, have smaller, slightly lanceolate wings, no sensilla and extra chaetae. Some alleles are embryonic lethal.
A study of the interactions between N, Dl, H and E(spl) suggest that the effects of H, Dl and E(spl) on N are allele specific and occurring at the protein level.
Functional relationships between neurogenic genes has been studied.
Bristles, especially postverticals and abdominals, missing in heterozygous H flies. Bristle sockets present at some sites, not at others. Expressed most distinctly on head; occipital; postvertical and ocellar bristles affected. Bristles of antennae and vibrissae show mutant phenotype much less frequently. Sockets without shafts also found on thorax, scutellum, abdominal tergites, external genitalia, wings, and legs. No shaftless sockets appear on the bracted costa of the wing. Some 40% of bristle organs located on distal part of femur differentiate neither shaft nor bract; bracts absent whenever shaft missing but present when shaft present; abnormally short shaft may be accompanied by normal-sized bract (from description of H2, by Tobler, Rothenbuhler and Nothiger (1973). Veins L4 and L5 do not reach wing margin; occasionally true of L2 also. Eyes larger than wild type; body color somewhat paler. Lees and Waddington (1942) show that trichogen cell forms a socket instead of a bristle shaft at some sites. Phenotypic expression of H responds linearly to dosage of Su(H)+ in region 35B6-10 on the left arm of chromosome 2. The number of microchaetae in H/+ flies varies from approximately 35 in the presence of a single dose of 35B6-10 to fewer than 10 in the presence of four doses (Ashburner, 1982). Interactions with other mutants studied by House (House, 1953a; House 1953b; House, 1959a; House, 1955; House, 1959b). H suppresses wing notching of N, fa, Nnd-3 and nd, enhances Ax; also H enhances eye effect of spl and removes more bristles in combination with spl (House, Von Halle). Reduction in the number of copies of the wild-type allele of H decreases the mutant phenotype of heterozygous N and Dl flies, but increase in the number of copies of the wild-type allele of H enhances the mutant phenotype of heterozygous N, Dl and E(spl) flies (Vassin, Vielmetter and Campos-Ortega, 1985). H shows some superadditive interaction with en, ci, ciW and ciD relative to degree of L4 interruption. L2 interruption augmented in combinations with ve and ri; L3 interruption augmented in combinations with ve and tt. Triploid, H/+/+, intermediate between wild type and H/+. H/H/+ most extreme type with bristles absent from head, thorax and abdomen (Gowen, 1933). Homozygous lethal. H null homozygotes die during larval and pupal stages (Bang, Hartenstein and Posakony, 1991). Animals surviving to pharate adult are completely devoid of macrochaetes and microchaetes on the head and notum, with occasional 'double sockets' remaining on the abdominal tergites. Bristles on the legs significantly resistant to loss of H+ function; many 'double sockets' and some normal bristles remain on the legs of H null homozygotes. In regions of the notum exhibiting bristle 'loss' in adult H mutants, macrochaete and microchaete primary precursor cells undetectable (Bang, Hartenstein and Posakony, 1991).