ArticleScientific reports2016
Novel Y-chromosomal microdeletions associated with non-obstructive azoospermia uncovered by high throughput sequencing of sequence-tagged sites (STSs).
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 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research progress on the role and mechanism of DNA damage repair in germ cell development.Frontiers in endocrinology · 2023Pooled it
- Human AZFb deletions cause distinct testicular pathologies depending on their extensions in Yq11 and the Y haplogroup: new cases and review of literature.Cell & bioscience · 2021Review
- Association of ESX1 gene variants with non-obstructive azoospermia in Chinese males.Scientific reports · 2021Article
- Y-Chromosome Microdeletions: A Review of Prevalence, Screening, and Clinical Considerations.The application of clinical genetics · 2021Review
- Deletion of b1/b3 shows risk for expanse of Yq microdeletion in male offspring: Case report of novel Y chromosome variations.Medicine · 2020Article
- Copy Number Variations in Female Infertility in China.Balkan journal of medical genetics : BJMG · 2019Article
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Authors and funding
24 authors.
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Abstract
Y-chromosomal microdeletion (YCM) serves as an important genetic factor in non-obstructive azoospermia (NOA). Multiplex polymerase chain reaction (PCR) is routinely used to detect YCMs by tracing sequence-tagged sites (STSs) in the Y chromosome. Here we introduce a novel methodology in which we sequence 1,787 (post-filtering) STSs distributed across the entire male-specific Y chromosome (MSY) in parallel to uncover known and novel YCMs. We validated this approach with 766 Chinese men with NOA and 683 ethnically matched healthy individuals and detected 481 and 98 STSs that were deleted in the NOA and control group, representing a substantial portion of novel YCMs which significantly influenced the functions of spermatogenic genes. The NOA patients tended to carry more and rarer deletions that were enriched in nearby intragenic regions. Haplogroup O2* was revealed to be a protective lineage for NOA, in which the enrichment of b1/b3 deletion in haplogroup C was also observed. In summary, our work provides a new high-resolution portrait of deletions in the Y chromosome.
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