The bithorax gene complex in Drosophila contains a minimum of eight genes that seem to code for substances controlling levels of thoracic and abdominal development. The state of repression of at least four of these genes is controlled by cis-regulatory elements and a separate locus (Polycomb) seems to code for a repressor of the complex. The wild-type and mutant segmentation patterns are consistent with an antero-posterior gradient in repressor concentration along the embryo and a proximo-distal gradient along the chromosome in the affinities for repressor of each gene's cis-regulatory element.

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The bithorax complex in Drosophila melanogaster is a cluster of homeotic genes that specify developmental pathways for many of the body segments of the fly. The DNA of the bithorax complex has been isolated, and a region of 195,000 base pairs that covers the left half of the complex is described here. The lesions associated with many of the bithorax complex mutants have been identified, and most are due to DNA rearrangements. Most of the spontaneous mutants have insertions of a particular mobile element named "gypsy." This element affects the functions of sequences removed from the site of insertion. Mutant lesions for a given phenotypic class are distributed over large DNA distances of up to 73,000 base pairs

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In Drosophila the Abdominal‐B (Abd‐B) domain of the bithorax complex (BX‐C) spans over 100 kb and is responsible for specifying the identities of adult abdominal segments five (A5) to nine (A9), inclusive, and correspondingly, neuromeres 10–14 of the embryonic central nervous system. The domain consists of a region coding for two proteins, ABD‐BI (54 kd) and ABD‐BII (36 kd) and cis‐regulatory regions extending from infra‐abdominal‐5 (iab‐5) to iab‐9, inclusive. We have used a monoclonal anti‐ABD‐B antibody to infer that mutants in iab‐8 eliminate the expression of ABD‐BI in neuromeres 10–13, inclusive, and that mutants in iab‐9 eliminate expression of ABD‐BII in neuromere 14. ABD‐B expression is also analyzed in homozygotes for (i) loss‐of‐function mutants involving the iab‐5, iab‐6 and iab‐7 regions, (ii) gain‐of‐function mutants Miscadastral pigmentation (Mcp) and Superabdominal (Sab), and (iii) a trans‐regulator, Polycomb (Pc). ABD‐B expression along the antero‐posterior axis is colinear with the chromosomal order of the cis‐regulatory regions. The behavior of rearrangement‐associated iab‐6 and iab‐7 mutants suggests that the enhancer‐like region, iab‐5, and possibly also iab‐6, may be shared between the abd‐A and Abd‐B domains. Such sharing is proposed as a factor that tends to keep gene complexes intact during evolution.