A TOP6BL mutation abolishes meiotic DNA double-strand break formation and causes human infertility.

Sci Bull (Beijing)

First Affiliated Hospital of University of Science and Technology of China, Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, CAS Center for Excellence in Molecular Cell Science, Collaborative Innovation Center of Genetics and Development, University of Science and Technology of China, Hefei 230027, China. Electronic address:

Published: December 2020

AI Article Synopsis

  • Meiosis is super important for making babies and helping with fertility, but not much research has been done on it in humans.
  • A family with four siblings had infertility problems, with three brothers unable to produce sperm and one sister having trouble getting pregnant, even though her ovaries looked normal.
  • Scientists found a mutation in a specific gene (TOP6BL) that caused these infertility issues, showing that without proper DNA break formation during meiosis, both male and female reproductive cells can’t develop correctly.

Article Abstract

Meiosis is pivotal for sexual reproduction and fertility. Meiotic programmed DNA double-strand breaks (DSBs) initiate homologous recombination, ensuring faithful chromosome segregation and generation of gametes. However, few studies have focused on meiotic DSB formation in human reproduction. Here, we report four infertile siblings born to a consanguineous marriage, with three brothers suffering from non-obstructive azoospermia and one sister suffering from unexplained infertility with normal menstrual cycles and normal ovary sizes with follicular activity. An autosomal recessive mutation in TOP6BL was found co-segregating with infertility in this family. Investigation of one male patient revealed failure in programmed meiotic DSB formation and meiotic arrest prior to pachytene stage of prophase I. Mouse models carrying similar mutations to that in patients recapitulated the spermatogenic abnormalities of the patient. Pathogenicity of the mutation in the female patient was supported by observations in mice that meiotic programmed DSBs failed to form in mutant oocytes and oocyte maturation failure due to absence of meiotic recombination. Our study thus illustrates the phenotypical characteristics and the genotype-phenotype correlations of meiotic DSB formation failure in humans.

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Source
http://dx.doi.org/10.1016/j.scib.2020.08.026DOI Listing

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