Rotte Nadja, Dunleavy Jessica E M, Runkel Michelle D, Bosse Lina, Fietz Daniela, Pilatz Adrian, Kuss Johanna, Dicke Ann-Kristin, Winge Sofia B, Di Persio Sara, Ruckert Christian, Nordhoff Verena, Schuppe Hans-Christian, Almstrup Kristian, Kliesch Sabine, Neuhaus Nina, Stallmeyer Birgit, O'Bryan Moira K, Tüttelmann Frank, Friedrich Corinna
Centre of Medical Genetics, Institute of Reproductive Genetics, University of Münster, 48149, Münster, Germany.
School of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, Faculty of Science, University of Melbourne, Parkville, VIC, 3010, Australia.
EMBO Mol Med. 2025 May 15. doi: 10.1038/s44321-025-00244-0.
Male infertility has been linked to M1AP. In mice, M1AP interacts with the ZZS proteins SHOC1/TEX11/SPO16, promoting DNA class I crossover formation during meiosis. To determine whether M1AP and ZZS proteins are involved in human male infertility by recombination failure, we screened for biallelic/hemizygous loss-of-function (LoF) variants in the human genes to select men with presumed protein deficiency (N = 24). After in-depth characterisation of testicular phenotypes, we identified gene-specific meiotic impairments: men with ZZS deficiency shared an early meiotic arrest. Men with LoF variants in M1AP exhibited a predominant metaphase I arrest with rare haploid round or even elongated spermatids. These differences were explained by different recombination failures: deficient ZZS function led to incorrect synapsis of homologous chromosomes, unrepaired DNA double-strand breaks, and incomplete recombination. Abolished M1AP led to a reduced number of recombination intermediates and class I crossover. Medically assisted reproduction resulted in the birth of a healthy child, offering the possibility of fatherhood to men with LoF variants in M1AP. Our study establishes M1AP as an important, but non-essential, functional enhancer in meiotic recombination.
男性不育与M1AP有关。在小鼠中,M1AP与ZZS蛋白SHOC1/TEX11/SPO16相互作用,促进减数分裂期间DNA I类交叉的形成。为了确定M1AP和ZZS蛋白是否因重组失败而导致人类男性不育,我们在人类基因中筛选了双等位基因/半合子功能丧失(LoF)变异,以选择可能存在蛋白质缺陷的男性(N = 24)。在对睾丸表型进行深入表征后,我们确定了基因特异性的减数分裂损伤:ZZS缺陷的男性共同存在早期减数分裂停滞。M1AP中存在LoF变异的男性表现出主要的中期I停滞,罕见单倍体圆形甚至拉长的精子细胞。这些差异可以通过不同的重组失败来解释:ZZS功能缺陷导致同源染色体的错误联会、未修复的DNA双链断裂和不完全重组。M1AP缺失导致重组中间体和I类交叉数量减少。医学辅助生殖使一名健康婴儿诞生,为M1AP中存在LoF变异的男性提供了成为父亲的可能性。我们的研究确定M1AP是减数分裂重组中一个重要但非必需的功能增强子。