Is a potent antagonist of neurogenic gene activity during sensory organ development. The expression of distinct cell fates by the trichogen (shaft) / tormogen (socket) sister cell pair depends on the level of H activity. A certain threshold level of H activity is required, below which both sister cells adopt the tormogen fate.

(UniProt, Q02308)

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; post vertical 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, Experientia 29: 370-71). 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, Proc. Roy. Soc. (London), Ser. B. 131: 87-110 (fig.)] 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, Genetics 64: 471-79). Interactions with other mutants studied by House (1953, Genetics 38: 199-215, 309-27; 1959, Genetics 44: 516; 1955, Anat. Record 122: 471; 1959, Anat. Record 134: 581-82). H suppresses wing notching of N, fa, fano, 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, J. Neurogenet. 2: 291-308). 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, Am. Nat. 67: 178-80 (fig.)]. Homozygous lethal. H null homozygotes die during larval and pupal stages (Bang et al.). 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 et al.). RK1.

Recessive allele of Hairy (formerly called Hairless-recessive). Homozygotes have nearly all bristles and hairs substituted by double and triple abnormal sockets; veins L4 and L5 fail to reach margin. H16/H lethal, probably in pupal stage; few escapers short lived with extreme Hairless phenotype; all bristles and hairs suppressed or substituted by abnormal sockets; wings reduced; veins L2, L4 and L5 abnormal.

Less severe than H16. Almost completely recessive. Heterozygotes most frequently wildtype in phenotype, but occasionally a "double socket" appears on the head in the position of a postvertical macrochaete or on the abdominal tergites. Homozygotes display a much stronger and more extensive mutant phenotype than H null heterozygotes. Many head and notum macrochaetes and approximately 50% of notum microchaetes missing; remaining 50% exhibit a spectrum of "double socket" phenotypes. Homozygotes also exhibit loss of wing vein tissue from L4 and L5. Approximately 50% of flies carrying H22r in trans to a H null allele die as pharate adults. The remainder survive to eclosion, but are short-lived and exhibit extensive loss of both macrochaetes and microchaetes on the head, notum, and abdominal tergites; only 20% of the notum microchaetes remain, all with a completely transformed "double socket" phenotype.