In(3R)hb^D2/hb¹² embryos exhibit a posterior cuticle and filzkorper defect.

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. hb^D2/ftz¹⁰); 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).