Detection of parent-of-origin effects for atopy by model-free and model-based linkage analyses.
Parent-of-origin effects for atopy were investigated by a model-free affected sib-pair (ASP) method and two model-based approaches in the Busselton nuclear families. Among the regions showing potential linkages to atopy by the ASP method, a significant excess of paternal allele sharing as compared with maternal allele sharing was observed for a cluster of three markers on chromosome 13. The two model-based methods, which specify either sex-specific recombination rates or different penetrances for heterozygotes according to the parental origin of disease allele (imprinting), led to the same results, both suggesting a paternal effect. Thus, these two ways of modelling parent-of-origin effects appear equivalent in nuclear family data. Further simulations are needed to investigate whether the mechanisms underlying parent-of-origin effects can be distinguished in larger pedigree structures.
Demenais
F
F
INSERM EMI 00-06, Hôpital Saint-Louis, Paris, France.
Chaudru
V
V
Martinez
M
M
D000328:Adult; D000483:Alleles; D001249:Asthma / Q000453:epidemiology / Q000235:genetics*; D001315:Australia; D002648:Child; D002874:Chromosome Mapping / Q000706:statistics & numerical data*; D002882:Chromosomes, Human, Pair 13; D005260:Female; D006580:Genetic Carrier Screening; D005819:Genetic Markers / Q000235:genetics*; D006801:Humans; D008297:Male; D008432:Mathematical Computing; D008957:Models, Genetic; D012130:Respiratory Hypersensitivity / Q000453:epidemiology / Q000235:genetics*
D005819:Genetic Markers