A de novo paradigm for male infertility

Nat Commun. 2022 Jan 10;13(1):154. doi: 10.1038/s41467-021-27132-8.

Abstract

De novo mutations are known to play a prominent role in sporadic disorders with reduced fitness. We hypothesize that de novo mutations play an important role in severe male infertility and explain a portion of the genetic causes of this understudied disorder. To test this hypothesis, we utilize trio-based exome sequencing in a cohort of 185 infertile males and their unaffected parents. Following a systematic analysis, 29 of 145 rare (MAF < 0.1%) protein-altering de novo mutations are classified as possibly causative of the male infertility phenotype. We observed a significant enrichment of loss-of-function de novo mutations in loss-of-function-intolerant genes (p-value = 1.00 × 10-5) in infertile men compared to controls. Additionally, we detected a significant increase in predicted pathogenic de novo missense mutations affecting missense-intolerant genes (p-value = 5.01 × 10-4) in contrast to predicted benign de novo mutations. One gene we identify, RBM5, is an essential regulator of male germ cell pre-mRNA splicing and has been previously implicated in male infertility in mice. In a follow-up study, 6 rare pathogenic missense mutations affecting this gene are observed in a cohort of 2,506 infertile patients, whilst we find no such mutations in a cohort of 5,784 fertile men (p-value = 0.03). Our results provide evidence for the role of de novo mutations in severe male infertility and point to new candidate genes affecting fertility.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Azoospermia / genetics*
  • Azoospermia / pathology
  • Case-Control Studies
  • Cell Cycle Proteins / deficiency
  • Cell Cycle Proteins / genetics*
  • DNA-Binding Proteins / deficiency
  • DNA-Binding Proteins / genetics*
  • Exome
  • Exome Sequencing
  • Gene Expression
  • Gene Expression Profiling
  • Genetic Predisposition to Disease*
  • Humans
  • Loss of Function Mutation*
  • Male
  • Mutation, Missense*
  • Oligospermia / genetics*
  • Oligospermia / pathology
  • RNA-Binding Proteins / genetics*
  • Tumor Suppressor Proteins / deficiency
  • Tumor Suppressor Proteins / genetics*

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • RBM5 protein, human
  • RNA-Binding Proteins
  • Tumor Suppressor Proteins