Institute of Biomedicine, University of Turku, Turku, Finland.
Natural Resources Institute Finland (Luke), Green Technology, Jokioinen, Finland.
Biol Reprod. 2017 Oct 1;97(4):522-536. doi: 10.1093/biolre/iox096.
Male infertility is an increasing problem partly due to inherited genetic variations. Mutations in genes involved in formation of the sperm tail cause motility defects and thus male infertility. Therefore, it is crucial to understand the protein networks required for sperm differentiation. Sperm motility is produced through activation of the sperm flagellum, which core structure, the axoneme, resembles motile cilia. In addition to this, cytoskeletal axonemal structure sperm tail motility requires various accessory structures. These structures are important for the integrity of the long tail, sperm capacitation, and generation of energy during sperm passage to fertilize the oocyte. This review discusses the current knowledge of mechanisms required for formation of the sperm tail structures and their effect on fertility. The recent research based on animal models and genetic variants in relation to sperm tail formation and function provides insights into the events leading to fertile sperm production. Here we compile a view of proteins involved in sperm tail development and summarize the current knowledge of factors contributing to reduced sperm motility, asthenozoospermia, underline the mechanisms which require further research, and discuss related clinical aspects on human male infertility.
男性不育症是一个日益严重的问题,部分原因是遗传基因突变。参与精子尾部形成的基因发生突变会导致运动缺陷,从而导致男性不育。因此,了解精子分化所需的蛋白质网络至关重要。精子的运动是通过精子鞭毛的激活产生的,其核心结构轴丝类似于运动纤毛。除此之外,精子尾部运动还需要各种辅助结构的细胞骨架轴丝结构。这些结构对于长尾巴的完整性、精子获能以及在精子通过受精卵子时产生能量非常重要。本文综述了精子尾部结构形成所需的机制及其对生育能力的影响。最近基于动物模型和与精子尾部形成和功能相关的遗传变异的研究为导致精子产生的事件提供了深入的了解。在这里,我们总结了参与精子尾部发育的蛋白质,并总结了导致精子运动能力降低、弱精症的因素的现有知识,强调了需要进一步研究的机制,并讨论了人类男性不育症的相关临床方面。