Genetic diversity of the human serotonin receptor 1B (HTR1B)

A. R. Sanders, Q. Cao, J. Taylor, T. E. Levin, J. A. Badner, A. Cravchik, J. M. Comeron, S. Naruya, A. Del Rosario, D. A. Salvi, K. A. Walczyk, L. R. Goldin, B. J. Mowry, D. F. Levinson, R. R. Crowe, J. M. Silverman, P. V. Gejman

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4 Scopus citations

Abstract

We extensively investigated polymorphisms in the coding and nearby non-coding regions of the intronless HTR1B, and their linkage disequilibrium relationships. By means of DGGE, database comparisons, and published assays, we have detected the following polymorphisms: G-511T, T-261G, -182INS/DEL-181, A-161T, C129T, T371G, T655C, C705T, G861C, A1099G, G1120A, and A1180G. The results of genotyping ten of these in an ethnic diversity panel (Pima/Jemez; Karatiana; Japanese; Chinese; Atayal; Indo-Pakistani; Middle Eastern; North of Sahara African; Mbutu/Biaka; Pacific Island; and European) revealed four common haplotypes: wild type, -182DEL-181, -161T, and 129T/861C. Gorilla and chimpanzee HTR1B sequence revealed the most common human alleles to be ancestral. One SNP, A-161T, had 108 transmissions of the A-161 allele to patients with schizophrenia versus 78 non-transmissions (nominal p=0.028). Nominal significance remained when linkage was controlled for by ASPEX/sib_tdt (p=0.041). Because many of the polymorphisms detected were uncommon, we also examined association of any variant allele with schizophrenia, which showed 222 transmissions versus 170 non-transmissions (nominal p=0.0086), and ASPEX/sib_tdt analysis (p=0.044). The expressed missense substitutions, T371G -> Phe124Cys, T655C -> Phe219Leu, A1099G -> Ile367Val, and G1120A -> Glu374Lys, could potentially affect ligand binding or interaction with G proteins, and thus modify drug response in carriers of these mutations.

Original languageEnglish
Pages (from-to)564
Number of pages1
JournalAmerican Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
Volume96
Issue number4
DOIs
StatePublished - 7 Aug 2000
Externally publishedYes

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