Deletion of the Spata3 Gene Induces Sperm Alterations and In Vitro Hypofertility in Mice.

Deletion of the Spata3 Gene Induces Sperm Alterations and In Vitro Hypofertility in Mice.
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Spata3基因缺失会导致小鼠精子改变和体外生育能力低下。

DOI:
10.3390/ijms22041959
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发表时间:
2021-02-16
影响因子:
5.6
通讯作者:
Barbaux S
Barbaux S
中科院分区:
生物学2区
文献类型:
--
作者:
Girault MS;Dupuis S;Ialy-Radio C;Stouvenel L;Viollet C;Pierre R;Favier M;Ziyyat A;Barbaux S

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通过对种间重组同源株 (IRCS) 的分析,我们之前将 Mafq1 数量性状位点定义为小鼠 1 号染色体上与雄性生育力低下和超微结构异常相关的区间。我们将精子发生相关蛋白 3 基因(Spata3 或 Tsarg1)确定为 Mafq1 位点内的相关候选基因,并通过 CRISPR-Cas9 介导的基因完全删除来研究其功能。删除 Spata3 的雄性小鼠在体内通常具有生育能力,但在体外受精测定中表现出效率急剧下降。流动性参数正常,但超微结构分析显示顶体缺陷和细胞质残留物中脂滴过多。因此,Spata3 基因的缺失部分地再现了生育能力低下的 IRCS 品系的表型。
Thanks to the analysis of an Interspecific Recombinant Congenic Strain (IRCS), we previously defined the Mafq1 quantitative trait locus as an interval on mouse Chromosome 1 associated with male hypofertility and ultrastructural abnormalities. We identified the Spermatogenesis associated protein 3 gene (Spata3 or Tsarg1) as a pertinent candidate within the Mafq1 locus and performed the CRISPR-Cas9 mediated complete deletion of the gene to investigate its function. Male mice deleted for Spata3 were normally fertile in vivo but exhibited a drastic reduction of efficiency in in vitro fertilization assays. Mobility parameters were normal but ultrastructural analyses revealed acrosome defects and an overabundance of lipids droplets in cytoplasmic remnants. The deletion of the Spata3 gene reproduces therefore partially the phenotype of the hypofertile IRCS strain.
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