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Such disorders can provide unique information concerning the genomic underpinnings of human neurodevelopment because effects of diametric variation in gene copy number on cognitive and behavioral phenotypes can be inferred. We describe evidence from the literature on deletions versus duplications for the regions underlying the best\u2010known human neurogenetic sister\u2010disorders, including Williams syndrome, Velocardiofacial syndrome, and Smith\u2013Magenis syndrome, as well as the X\u2010chromosomal conditions Klinefelter and Turner syndromes. These data suggest that diametric copy\u2010number alterations can, like diametric alterations to imprinted genes, generate contrasting phenotypes associated with autistic\u2010spectrum and psychotic\u2010spectrum conditions. Genomically based perturbations to the development of the human social brain are thus apparently mediated to a notable degree by effects of variation in gene copy number. We also conducted the first analyses of positive selection for genes in the regions affected by these disorders. We found evidence consistent with adaptive evolution of protein\u2010coding genes, or selective sweeps, for three of the four sets of sister\u2010syndromes analyzed. These studies of selection facilitate identification of candidate genes for the phenotypes observed and lend a novel evolutionary dimension to the analysis of human cognitive architecture and neurogenetic disorders.<\/jats:p>","DOI":"10.1111\/j.1752-4571.2008.00056.x","type":"journal-article","created":{"date-parts":[[2009,1,7]],"date-time":"2009-01-07T09:55:58Z","timestamp":1231322158000},"page":"81-100","source":"Crossref","is-referenced-by-count":31,"title":["ORIGINAL ARTICLE: Genomic sister\u2010disorders of neurodevelopment: an evolutionary 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