Many loci, such as the bithorax complex referred to earlier, exhibit a genetic phenomenon called “transvection,” whereby a wild-type regulatory region upstream of a defective protein-coding sequence on one chromosome can rescue a relatively normal phenotype, when it is combined with a mutant regulatory region linked to a wild-type protein-coding sequence on the homologous chromosome (both of which give mutant phenotypes when homozygous) [130]. This phenomenon is well documented in Drosophila but appears to occur in most animals and has been interpreted as a physical cross-talk between functional cis-acting promoters or enhancers on one chromosome to engender transcription of adjacent protein-coding genes on the other, since the effect is usually pairing-dependent and lost when the regulatory and protein-coding sequences are separated to nonsyntenic positions in the genome [130],[148]. However, this is not always the case—at some loci, transvection between regulatory elements and protein-coding sequences can operate over large distances (even between different chromosomes) [149]–[152], suggesting the involvement of a trans-acting signal. Moreover, many promoter elements that exhibit transvection are transcribed into ncRNAs, and transvection is altered in Polycomb and zeste
