ArticleScientific reports2016
Y chromosome haplogroups based genome-wide association study pinpoints revelation for interactions on non-obstructive azoospermia.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Research progress on the fanconi anemia signaling pathway in non-obstructive azoospermia.Frontiers in endocrinology · 2024Review
- Evaluation of Male Fertility-Associated Loci in a European Population of Patients with Severe Spermatogenic Impairment.Journal of personalized medicine · 2020Article
- Review
- High Levels of Copy Number Variation of Ampliconic Genes across Major Human Y Haplogroups.Genome biology and evolution · 2018Article
- Viewing the male-specific chromosome Y in a new light.European journal of human genetics : EJHG · 2017Article
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Authors and funding
16 authors at 3 institutions in 1 country.
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Abstract
The Y chromosome has high genetic variability with low rates of parallel and back mutations, which make up the most informative haplotyping system. To examine whether Y chromosome haplogroups (Y-hgs) could modify the effects of autosomal variants on non-obstructive azoospermia (NOA), based on our previous genome-wide association study (GWAS), we conducted a genetic interaction analysis in GWAS subjects. Logistic regression analysis demonstrated a protective effect of Y-hg O3e(*) on NOA. Then, we explored the potential interaction between Y-hg O3e(*) and autosomal variants. Our results demonstrated that there was a suggestively significant interaction between Y-hg O3e(*) and rs11135484 on NOA (Pinter = 9.89 × 10(-5)). Bioinformatic analysis revealed that genes annotated by significant single nucleotide polymorphisms (SNPs) were mainly enriched in immunological pathways. This is the first study of interactions between Y-hgs and autosomal variants on a genome-wide scale, which addresses the missing heritability in spermatogenic impairment and sheds new light on the pathogenesis of male infertility.
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