Genetic Epidemiology, Psychiatric Genetics, Asthma Genetics and Statistical Genetics Laboratories investigate the pattern of disease in families, particularly identical and non-identical twins, to assess the relative importance of genes and environment in a variety of important health problems.
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PMID
10999839
TITLE
Dizygotic twinning is not linked to variation at the alpha-inhibin locus on human chromosome 2.
ABSTRACT
Natural multiple pregnancy in women leading to dizygotic (DZ) twins is familial and varies across racial groups, suggesting a genetic predisposition. Mothers of DZ twins have a higher incidence of spontaneous multiple ovulation and elevated FSH concentrations. FSH release is controlled by feedback of inhibin peptides from the ovary, and immunization against inhibin alpha-subunit results in an increased ovulation rate in animals. The inhibin alpha-subunit is therefore a candidate gene for mutations that may increase the frequency of DZ twinning. Restriction digests of a PCR product from exon 1 with the enzyme SpeI detects a C/T polymorphism at bp 128 with two alleles of 447 and 323/124 bp. The polymorphism was typed in 1,125 individuals from 326 pedigrees with 717 mothers of spontaneous DZ twins. The alpha-inhibin locus mapped within 3 centimorgans of D2S164, and linkage with DZ twinning was excluded [decimal log odds ratio (LOD) score, -2.81 at theta = 0]. There was complete exclusion of linkage (LOD, less than -2) of a gene conferring relative risk 1.8 (lambdas, >1.8) across the chromosome, except at the p-terminus region and a small peak (maximum LOD score, 0.6) in the region of D2S151-D2S326. Analysis using either recessive or dominant models excluded linkage with DZ twinning in this population (LOD score, less than -2.5) across chromosome 2. We conclude that dizygotic twinning is not linked to variation in the alpha-inhibin locus. The results also suggest that mutations in other candidates on chromosome 2, including the receptor for FSH and the betaB-inhibin subunit (INHBB) cannot be major contributors to risk for DZ twinning.
DATE PUBLISHED
2000 Sep
HISTORY
PUBSTATUS PUBSTATUSDATE
pubmed 2000/09/22 11:00
medline 2000/10/21 11:01
entrez 2000/09/22 11:00
AUTHORS
NAME COLLECTIVENAME LASTNAME FORENAME INITIALS AFFILIATION AFFILIATIONINFO
Montgomery GW Montgomery G W GW Genetic Epidemiology Laboratory, Queensland Institute of Medical Research and Joint Genetics Program, University of Queensland, Brisbane, Australia. grantM@qimr.edu.au
Duffy DL Duffy D L DL
Hall J Hall J J
Haddon BR Haddon B R BR
Kudo M Kudo M M
McGee EA McGee E A EA
Palmer JS Palmer J S JS
Hsueh AJ Hsueh A J AJ
Boomsma DI Boomsma D I DI
Martin NG Martin N G NG
INVESTIGATORS
JOURNAL
VOLUME: 85
ISSUE: 9
TITLE: The Journal of clinical endocrinology and metabolism
ISOABBREVIATION: J. Clin. Endocrinol. Metab.
YEAR: 2000
MONTH: Sep
DAY:
MEDLINEDATE:
SEASON:
CITEDMEDIUM: Print
ISSN: 0021-972X
ISSNTYPE: Print
MEDLINE JOURNAL
MEDLINETA: J Clin Endocrinol Metab
COUNTRY: United States
ISSNLINKING: 0021-972X
NLMUNIQUEID: 0375362
PUBLICATION TYPE
PUBLICATIONTYPE TEXT
Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't
Twin Study
COMMENTS AND CORRECTIONS
GRANTS
GENERAL NOTE
KEYWORDS
MESH HEADINGS
DESCRIPTORNAME QUALIFIERNAME
Chromosome Mapping
Chromosomes, Human, Pair 2 genetics
DNA genetics
Exons genetics
Female genetics
Genetic Linkage genetics
Genome genetics
Humans genetics
Inhibins genetics
Pedigree genetics
Polymorphism, Genetic genetics
Pregnancy genetics
Receptors, FSH genetics
Reverse Transcriptase Polymerase Chain Reaction genetics
Twins, Dizygotic genetics
SUPPLEMENTARY MESH
GENE SYMBOLS
CHEMICALS
REGISTRYNUMBER NAMEOFSUBSTANCE
0 Receptors, FSH
57285-09-3 Inhibins
9007-49-2 DNA
OTHER ID's