Gene Dmel\hb

Homozygotes for null alleles of hb (class I alleles of Lehmann and Nusslein-Volhard) are embryonic lethals of the gap type. Gastrulation abnormal; no cephalic fold; cell death evident at 6 hr later becoming extensive, predominantly in the neuroectoderm; germ band extension curtailed at 50% of embryonic length. After germ band shortening embryos lack thoracic and labial segments; cephalopharyngeal skeleton present but poorly formed; head involution fails. Seventh and eighth abdominal segments fused by the deletion of parasegment 13; A1 segment 1.5 times normal width, with eight to ten deranged denticle rows compared to the normal number of four, and a widened region of naked cuticle. Filzkorper material reduced; posterior spiracles fail to evert. Three ventral ganglia absent; gap appears between suboesophogeal region of ventral nerve cord and more posterior trunk ganglia. Extreme mutants display a reduced number of stripes of ftz expression at cellular blastoderm; the first stripe is widened and followed by a narrowed gap of nonexpression preceding the second stripe; the last pair of stripes are fused (Carroll and Scott, 1986, Cell 45: 113-26). Hypomorphic alleles display variably less severe disruption depending on allele (hbDrv6 = hbb2 = hbe21 > hbb7 > hbDrv9), the least severe, hbDrv9 lacking only T2. Class II alleles (Lehmann and Nusslein-Volhard) resemble the null alleles except that some or all of the prothorax and A7 are retained. The class III allele retains the labial segment as well. Class IV alleles lack only the mesothoracic segment. Class V mutants exhibit segment transformations as well as gaps and are described separately below. Temperature sensitive period of hbts1 during first four hr of development. hb/+ offspring produced from homozygous oogenic clones develop normally; homozygous embryos resulting from such clones display enhanced zygotic phenotype; gnathal, thoracic, and the first three abdominal segments replaced by two or three segments of abdominal identity in mirror image relation to the more posterior abdominal segments; weak alleles without maternal effect; extra doses of hb+ in female without effect on phenotype of hb offspring. The anterior zone of hb expression extended posteriorly by six additional cells in the absence of Kr+; conversely the zone of Kr expression expanded anteriorly by six to eight cells in hb mutants; posterior zone appears insensitive to Kr constitution (Jackle, Tautz, Schuh, Seifert, and Lehmann, 1986, Nature 324: 668-70). hb+ appears to set the boundaries of Ubx expression (White and Lehmann, 1986, Cell 47: 311-21); zone of Ubx expression expanded in both anterior and posterior directions in hb mutant embryos at the stage of full germ band elongation; segmental disposition of expression characteristically deranged prior to the advent of cell death. Although Ubx expression in the ventral nerve chord at the stage of fully shortened germ band extends from parasegments 5-13, Ubx protein detected in parasegments 1, 7-12 and 14 in hb12, 3 and 7-14 in hb1, and head to parasegment 1 plus parasegments 7-12 and 14 in hb7 (White and Lehmann). Phenotypic effects of ftz and hb in double mutants additive in thorax and anterior abdomen, but more severe than expected in head and posterior regions.

hb6/hb6 embryos lack meso- and metathorax, but nine abdominal segments are formed, the most anterior being T2 transformed into A1 and the next the normal A1.

Homozygous embryos lack labium and all thoracic segments; head and gnathal segments transformed into posterior abdominal segments as is A1. Expressed only in homozygotes, not in hemizygotes; hb7/Df(3R)hb displays class III phenotype. Lethality of hb7 homozygotes not rescued by Dp(3;Y)P92 which is able to cover the other alleles; attempts to implicate a linked lethal mutation negative.

As in the case of hb7, resembles a class I mutant, but with transformation of gnathal and first abdominal segments into posterior abdominal segments. Expression in homozygotes more extreme than in hemizygotes.

A gain-of-function mutation; viable both in heterozygous and homozygous condition. Phenotype resembles that of pbx; insensitive to additional doses of hb+ but suppressed by extra doses [e. g., five copies of BXC+ (Lewis)]; enhanced in heterozygous combination with null alleles of ftz.

Homozygous lethal; lethal when heterozygous to hb null alleles (e.g. hb12). Has two dominant phenotypes: 1) homeotic transformation of parasegment six to parasegment five, resembling that produced by bxd pbx; 2) a pair-rule segmentation defect, consisting of partial deletion of even-numbered abdominal segments, principally A2 and A4. Homozygote shows more extreme expression of both phenotypes; penetrance and expressivity of first effect enhanced in double heterozygous combination with null alleles of ftz (e.g. hbD2/ftzr14); second phenotype enhanced by Df(2R)eve, such that only a few adult escapers of the doubly heterozygous genotype are observed. Also has a recessive phenotype, revealed either when homozygous or heterozygous to an hb null allele; deletion of parasegment 13 and reduction of filzkorper; labial and thoracic segments normal. Thus, affects posterior, but not anterior, domain of hb+ function. Viable in trans to some hypomorphic alleles that do not affect parasegment 13 (e.g. hb6).