Fine mapping of a susceptibility locus for bipolar and genetically related unipolar affective disorders, to a region containing the C21ORF29 and TRPM2 genes on chromosome 21q22.3

Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried out tests of allelic association using 30 genetic markers near the telomere at 21q22.3 in 600 bipolar research subjects and 450 ancestrally...

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Published inMolecular psychiatry Vol. 11; no. 2; pp. 134 - 142
Main Authors McQuillin, A, Bass, N J, Kalsi, G, Lawrence, J, Puri, V, Choudhury, K, Detera-Wadleigh, S D, Curtis, D, Gurling, H M D
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.02.2006
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Abstract Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried out tests of allelic association using 30 genetic markers near the telomere at 21q22.3 in 600 bipolar research subjects and 450 ancestrally matched supernormal control subjects. We found significant allelic association with the microsatellite markers D21S171 ( P =0.016) and two closely linked single-nucleotide polymorphisms, rs1556314 ( P =0.008) and rs1785467 ( P =0.025). A test of association with a three locus haplotype across the susceptibility region was significant with a permutation test of P =0.011. A two SNP haplotype was also significantly associated with bipolar disorder ( P =0.01). Only two brain expressed genes, TRPM2 and C21ORF29 (TSPEAR), are present in the associated region. TRPM2 encodes a calcium channel receptor and TSPEAR encodes a peptide with repeats associated with epilepsy in the mouse. DNA from subjects who had inherited the associated marker alleles was sequenced. A base pair change (rs1556314) in exon 11 of TRPM2, which caused a change from an aspartic acid to a glutamic acid at peptide position 543 was found. This SNP showed the strongest association with bipolar disorder ( P =0.008). Deletion of exon 11 of TRPM2 is known to cause dysregulation of cellular calcium homeostasis in response to oxidative stress. A second nonconservative change from arginine to cysteine at position 755 in TRPM2 (ss48297761) was also detected. A third nonconservative change from histidine to glutamic acid was found in exon 8 of TSPEAR. These changes need further investigation to establish any aetiological role in bipolar disorder.
AbstractList Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried out tests of allelic association using 30 genetic markers near the telomere at 21q22.3 in 600 bipolar research subjects and 450 ancestrally matched supernormal control subjects. We found significant allelic association with the microsatellite markers D21S171 (P=0.016) and two closely linked single-nucleotide polymorphisms, rs1556314 (P=0.008) and rs1785467 (P=0.025). A test of association with a three locus haplotype across the susceptibility region was significant with a permutation test of P=0.011. A two SNP haplotype was also significantly associated with bipolar disorder (P=0.01). Only two brain expressed genes, TRPM2 and C21ORF29 (TSPEAR), are present in the associated region. TRPM2 encodes a calcium channel receptor and TSPEAR encodes a peptide with repeats associated with epilepsy in the mouse. DNA from subjects who had inherited the associated marker alleles was sequenced. A base pair change (rs1556314) in exon 11 of TRPM2, which caused a change from an aspartic acid to a glutamic acid at peptide position 543 was found. This SNP showed the strongest association with bipolar disorder (P=0.008). Deletion of exon 11 of TRPM2 is known to cause dysregulation of cellular calcium homeostasis in response to oxidative stress. A second nonconservative change from arginine to cysteine at position 755 in TRPM2 (ss48297761) was also detected. A third nonconservative change from histidine to glutamic acid was found in exon 8 of TSPEAR. These changes need further investigation to establish any aetiological role in bipolar disorder.
Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried out tests of allelic association using 30 genetic markers near the telomere at 21q22.3 in 600 bipolar research subjects and 450 ancestrally matched supernormal control subjects. We found significant allelic association with the microsatellite markers D21S171 ( P =0.016) and two closely linked single-nucleotide polymorphisms, rs1556314 ( P =0.008) and rs1785467 ( P =0.025). A test of association with a three locus haplotype across the susceptibility region was significant with a permutation test of P =0.011. A two SNP haplotype was also significantly associated with bipolar disorder ( P =0.01). Only two brain expressed genes, TRPM2 and C21ORF29 (TSPEAR), are present in the associated region. TRPM2 encodes a calcium channel receptor and TSPEAR encodes a peptide with repeats associated with epilepsy in the mouse. DNA from subjects who had inherited the associated marker alleles was sequenced. A base pair change (rs1556314) in exon 11 of TRPM2, which caused a change from an aspartic acid to a glutamic acid at peptide position 543 was found. This SNP showed the strongest association with bipolar disorder ( P =0.008). Deletion of exon 11 of TRPM2 is known to cause dysregulation of cellular calcium homeostasis in response to oxidative stress. A second nonconservative change from arginine to cysteine at position 755 in TRPM2 (ss48297761) was also detected. A third nonconservative change from histidine to glutamic acid was found in exon 8 of TSPEAR. These changes need further investigation to establish any aetiological role in bipolar disorder.
Audience Academic
Author Lawrence, J
Choudhury, K
Detera-Wadleigh, S D
Kalsi, G
Gurling, H M D
Curtis, D
Puri, V
Bass, N J
McQuillin, A
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Keywords manic depression
genetic susceptibility
chromosome 21
linkage disequilibrium
Language English
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SSID ssj0014765
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Snippet Linkage analyses of bipolar families have confirmed that there is a susceptibility locus near the telomere on chromosome 21q. To fine map this locus we carried...
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StartPage 134
SubjectTerms Affective disorders
Amino Acid Substitution
Aspartic acid
Behavioral Sciences
Biological Psychology
Bipolar disorder
Bipolar Disorder - genetics
Calcium homeostasis
Case-Control Studies
Chromosome 21
Chromosome Mapping
Chromosomes, Human, Pair 21 - genetics
Epilepsy
Gene mapping
Genetic markers
Genetic Predisposition to Disease - genetics
Glutamic acid
Haplotypes
Histidine
Homeostasis
Humans
Linkage Disequilibrium
Medicine
Medicine & Public Health
Microsatellite Repeats - genetics
Microsatellites
Mood Disorders - genetics
Neurosciences
Nucleotide sequence
original-article
Oxidative stress
Pedigree
Peptides
Pharmacotherapy
Polymorphism, Genetic
Psychiatry
Single-nucleotide polymorphism
Susceptibility
Telomeres
Transient receptor potential proteins
TRPM Cation Channels - genetics
Title Fine mapping of a susceptibility locus for bipolar and genetically related unipolar affective disorders, to a region containing the C21ORF29 and TRPM2 genes on chromosome 21q22.3
URI http://dx.doi.org/10.1038/sj.mp.4001759
https://link.springer.com/article/10.1038/sj.mp.4001759
https://www.ncbi.nlm.nih.gov/pubmed/16205735
https://www.proquest.com/docview/221169135
https://www.proquest.com/docview/2645758300
https://search.proquest.com/docview/70729763
Volume 11
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