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Rare mutations in the complement regulatory gene CSMD1 are associated with male and female infertility

Author

Listed:
  • Arthur S. Lee

    (Washington University School of Medicine)

  • Jannette Rusch

    (Washington University School of Medicine)

  • Ana C. Lima

    (Washington University School of Medicine)

  • Abul Usmani

    (Washington University School of Medicine)

  • Ni Huang

    (Washington University School of Medicine)

  • Maarja Lepamets

    (University of Tartu)

  • Katinka A. Vigh-Conrad

    (Oregon Health and Science University)

  • Ronald E. Worthington

    (Southern Illinois University)

  • Reedik Mägi

    (University of Tartu)

  • Xiaobo Wu

    (Washington University School of Medicine)

  • Kenneth I. Aston

    (University of Utah School of Medicine)

  • John P. Atkinson

    (Washington University School of Medicine)

  • Douglas T. Carrell

    (University of Utah School of Medicine)

  • Rex A. Hess

    (University of Illinois)

  • Moira K. O’Bryan

    (Monash University)

  • Donald F. Conrad

    (Washington University School of Medicine
    Oregon Health and Science University
    Oregon Health and Sciences University)

Abstract

Infertility in men and women is a complex genetic trait with shared biological bases between the sexes. Here, we perform a series of rare variant analyses across 73,185 women and men to identify genes that contribute to primary gonadal dysfunction. We report CSMD1, a complement regulatory protein on chromosome 8p23, as a strong candidate locus in both sexes. We show that CSMD1 is enriched at the germ-cell/somatic-cell interface in both male and female gonads. Csmd1-knockout males show increased rates of infertility with significantly increased complement C3 protein deposition in the testes, accompanied by severe histological degeneration. Knockout females show significant reduction in ovarian quality and breeding success, as well as mammary branching impairment. Double knockout of Csmd1 and C3 causes non-additive reduction in breeding success, suggesting that CSMD1 and the complement pathway play an important role in the normal postnatal development of the gonads in both sexes.

Suggested Citation

  • Arthur S. Lee & Jannette Rusch & Ana C. Lima & Abul Usmani & Ni Huang & Maarja Lepamets & Katinka A. Vigh-Conrad & Ronald E. Worthington & Reedik Mägi & Xiaobo Wu & Kenneth I. Aston & John P. Atkinson, 2019. "Rare mutations in the complement regulatory gene CSMD1 are associated with male and female infertility," Nature Communications, Nature, vol. 10(1), pages 1-16, December.
  • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-12522-w
    DOI: 10.1038/s41467-019-12522-w
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    Cited by:

    1. Wei Yang & Li-Bo Liu & Feng-Liang Liu & Yan-Hua Wu & Zi-Da Zhen & Dong-Ying Fan & Zi-Yang Sheng & Zheng-Ran Song & Jia-Tong Chang & Yong-Tang Zheng & Jing An & Pei-Gang Wang, 2023. "Single-cell RNA sequencing reveals the fragility of male spermatogenic cells to Zika virus-induced complement activation," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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