Genes and duplicons in genomic disorders involving complex duplicons. (a) 7q11.23 deletions in WS; (b) reciprocal 17p11.2 deletions in SMS and duplications in duplication 17p11.2 syndrome; (c) 22q11 deletions in DiGeorge and VCFS syndromes; (d) common deletions in the imprinted PWS and AS. Duplicons, unequal crossing-over positions, as well as frequency, genes, and abbreviations, are denoted as in Fig. 2. Triangles pointing in both directions reflect the complex modules revealed by 22q11 sequence. A major gene contributing to Williams syndrome,elastin, is shown as a hatched rectangle, as is theUBE3A gene involved in Angelman syndrome (AS). Genes that contribute to Smith-Magenis, duplication 17p11.2, DiGeorge/VCFS, and Prader-Willi syndromes are unknown. (See text for references.)