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细胞质内的轴丝动力蛋白臂组装缺陷导致精子细胞形态异常和运动能力下降,从而导致男性不育。

Defects in the cytoplasmic assembly of axonemal dynein arms cause morphological abnormalities and dysmotility in sperm cells leading to male infertility.

机构信息

Department of General Pediatrics, University Hospital Muenster, Muenster, Germany.

Institute of Reproductive Genetics, University of Muenster, Muenster, Germany.

出版信息

PLoS Genet. 2021 Feb 26;17(2):e1009306. doi: 10.1371/journal.pgen.1009306. eCollection 2021 Feb.

Abstract

Axonemal protein complexes, such as outer (ODA) and inner (IDA) dynein arms, are responsible for the generation and regulation of flagellar and ciliary beating. Studies in various ciliated model organisms have shown that axonemal dynein arms are first assembled in the cell cytoplasm and then delivered into axonemes during ciliogenesis. In humans, mutations in genes encoding for factors involved in this process cause structural and functional defects of motile cilia in various organs such as the airways and result in the hereditary disorder primary ciliary dyskinesia (PCD). Despite extensive knowledge about the cytoplasmic assembly of axonemal dynein arms in respiratory cilia, this process is still poorly understood in sperm flagella. To better define its clinical relevance on sperm structure and function, and thus male fertility, further investigations are required. Here we report the fertility status in different axonemal dynein preassembly mutant males (DNAAF2/ KTU, DNAAF4/ DYX1C1, DNAAF6/ PIH1D3, DNAAF7/ZMYND10, CFAP300/C11orf70 and LRRC6). Besides andrological examinations, we functionally and structurally analyzed sperm flagella of affected individuals by high-speed video- and transmission electron microscopy as well as systematically compared the composition of dynein arms in sperm flagella and respiratory cilia by immunofluorescence microscopy. Furthermore, we analyzed the flagellar length in dynein preassembly mutant sperm. We found that the process of axonemal dynein preassembly is also critical in sperm, by identifying defects of ODAs and IDAs in dysmotile sperm of these individuals. Interestingly, these mutant sperm consistently show a complete loss of ODAs, while some respiratory cilia from the same individual can retain ODAs in the proximal ciliary compartment. This agrees with reports of solely one distinct ODA type in sperm, compared to two different ODA types in proximal and distal respiratory ciliary axonemes. Consistent with observations in model organisms, we also determined a significant reduction of sperm flagellar length in these individuals. These findings are relevant to subsequent studies on the function and composition of sperm flagella in PCD patients and non-syndromic infertile males. Our study contributes to a better understanding of the fertility status in PCD-affected males and should help guide genetic and andrological counselling for affected males and their families.

摘要

轴丝蛋白复合物,如外(ODA)和内(IDA)动力臂,负责产生和调节鞭毛和纤毛的运动。在各种纤毛模型生物中的研究表明,轴丝动力臂首先在细胞质中组装,然后在纤毛发生期间输送到轴丝中。在人类中,编码参与该过程的因子的基因突变导致各种器官(如气道)中的运动纤毛的结构和功能缺陷,并导致遗传性疾病原发性纤毛运动障碍(PCD)。尽管关于呼吸纤毛中轴丝动力臂的细胞质组装有广泛的了解,但在精子鞭毛中这一过程仍知之甚少。为了更好地定义其对精子结构和功能的临床相关性,从而定义男性生育能力,需要进一步的研究。在这里,我们报告了不同轴丝动力臂预组装突变体男性(DNAAF2/ KTU、DNAAF4/ DYX1C1、DNAAF6/ PIH1D3、DNAAF7/ZMYND10、CFAP300/C11orf70 和 LRRC6)的生育状况。除了男科检查外,我们还通过高速视频和透射电子显微镜对受影响个体的精子鞭毛进行了功能和结构分析,并通过免疫荧光显微镜系统比较了精子鞭毛和呼吸纤毛中动力臂的组成。此外,我们还分析了动力臂预组装突变体精子的鞭毛长度。我们发现,在这些个体的运动能力差的精子中,轴丝动力臂的预组装过程也是至关重要的,因为发现了 ODAs 和 IDAs 的缺陷。有趣的是,这些突变精子始终完全丧失了 ODAs,而同一个体的一些呼吸纤毛在近端纤毛隔室中仍保留 ODAs。这与精子中仅有一种独特的 ODA 类型的报道一致,而在近端和远端呼吸纤毛轴丝中则有两种不同的 ODA 类型。与模型生物中的观察结果一致,我们还确定这些个体的精子鞭毛长度显著缩短。这些发现与随后在 PCD 患者和非综合征性不育男性的精子鞭毛功能和组成研究相关。我们的研究有助于更好地了解 PCD 受影响男性的生育状况,并应有助于指导受影响男性及其家属的遗传和男科咨询。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e1/7909641/382324f3113d/pgen.1009306.g001.jpg

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