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Genetics, Vol. 167, 1833-1840, August 2004, Copyright © 2004
doi:10.1534/genetics.104.028217
A Genetic Mechanism Implicates Chromosome 11 in Schizophrenia and Bipolar Diseases
Amar J. S. Klar1
Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702-1201
1 Address for correspondence: Laboratory of Eukaryotic Gene Expression, National Cancer Institute, P.O. Box B, Frederick, MD 21702-1201.
E-mail: klar{at}ncifcrf.gov
The causes of schizophrenia and bipolar human psychiatric disorders are unknown. A novel somatic cell genetic model postulated nonrandom segregation of "Watson" vs. "Crick" DNA chains of both copies of a chromosome to specific daughter cells. Such an oriented asymmetric cell division causes development of healthy, functionally nonequivalent brain hemispheres. Genetic translocations of the chromosome may cause disease by disrupting the biased strand-segregation process. Only one-half of chromosome 1 and 11 translocation carriers developing disease were recently explained as a result consistent with the model (KLAR 2002). Is chromosome 1 or 11 involved? Does the translocation breakpoint cause disease? Remarkably, two other unrelated chromosome 11 translocations discovered from the literature likewise caused disease in 
50% of carriers. Together, their breakpoints lie at three distinct regions spanning 40% of chromosome 11. Thus, chromosome 11 is implicated but the breakpoints themselves are unlikely to cause the disease. The results suggest that the genetically caused disease develops without a Mendelian gene mutation.
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