CCG repeats in cDNAs from human brain

Expansion mutations of trinucleotide repeats and other units of unstable DN A have been proposed to account for at least some of the genetic susceptibi lity to a number of neuropsychiatric disorders, including bipolar affective disorder, schizophrenia, autism, and panic disorder. To generate additiona l candidate genes for these and other disorders, cDNA libraries from human brain were probed at high stringency for clones containing CCG, CGC, GCC, C GG, GCG, and GGC repeats (referred to collectively as CCG repeats). Some 18 cDNAs containing previously unpublished or uncharacterized repeats were ch aracterized for chromosomal locus, repeat length polymorphism, and similari ty to genes of known function. The cDNAs were also compared with the 37 hum an genes with eight or more consecutive CCG triplets in GenBank. The repeat s were mapped to a number of loci, including 1p34, 2p11.2, 2q30-32 3p21, 3p 22, 4q35, 6q22, 7qter, 13p13, 17q24, 18p11, 14p13.3, 20q12, 20q13.3, and 22 q12. Length polymorphism was detected in 50% of the repeats. The newly clon ed cDNAs in elude a complete transcript of human neurexin-1B, a portion of BCNG-1 (a newly described brain-specific ion channel), a previously unrepor ted polymolphic repeat located in the 5' UTR legion of the guanine nucleoti de-binding protein (G-protein) beta 2 subunit, and a human version of the m ouse proline-rich protein 7. This list of cDNAs should expedite the search for expansion mutations associated with diseases of the central nervous sys tem.