锌指RNA结合蛋白2（ZFR2）对小鼠雄性生育能力并非必需。
Zinc finger RNA binding protein 2 (ZFR2) is not required for male fertility in the mouse.
作者信息
Cauchi Lachlan M, Houston Brendan J, Nagirnaja Liina, O'Connor Anne E, Merriner D Jo, Aston Kenneth I, Schlegel Peter N, Conrad Don F, Burke Richard, O'Bryan Moira K
机构信息
School of Biological Sciences, Monash University, Clayton, Australia; Institute for Veterinary Anatomy, Histology and Embryology, Justus-Liebig University, Giessen, Germany.
The School of BioSciences and Bio21 Institute, The University of Melbourne, Parkville, Australia.
出版信息
Dev Biol. 2022 Sep;489:55-61. doi: 10.1016/j.ydbio.2022.05.020. Epub 2022 Jun 6.
BACKGROUND
Thousands of genes are expressed during spermatogenesis and male infertility has a strong genetic component. Within this study, we focus on the role of Zfr2 in male fertility, a gene previously implicated in human male fertility. To date, very little is known about the role of ZFR2 in either humans or mice. To this end, the requirement for ZFR2 in male fertility was assessed using a knockout mouse model.
RESULTS
Zfr2 was found to be expressed in the testes of both humans and mice. Deletion of Zfr2 was achieved via removal of exon 2 using CRISPR-Cas9 methods. The absence of Zfr2 did not result in a reduction in any fertility parameters assessed. Knockout males were capable of fostering litter sizes equal to wild type males, and there were no effects of Zfr2 knockout on sperm number or motility. We note Zfr2 knockout females were also fertile.
CONCLUSIONS
The absence of Zfr2 alone is not sufficient to cause a reduction in male fertility in mice.
背景
在精子发生过程中有数千个基因表达，男性不育具有很强的遗传因素。在本研究中，我们聚焦于Zfr2在男性生育中的作用，该基因先前被认为与人类男性生育有关。迄今为止，关于ZFR2在人类或小鼠中的作用知之甚少。为此，我们使用基因敲除小鼠模型评估了Zfr2在男性生育中的必要性。
结果
发现Zfr2在人类和小鼠的睾丸中均有表达。通过使用CRISPR-Cas9方法去除外显子2实现了Zfr2的缺失。Zfr2的缺失并未导致所评估的任何生育参数降低。基因敲除雄性能够养育与野生型雄性相当的窝仔数，并且Zfr2基因敲除对精子数量或活力没有影响。我们注意到Zfr2基因敲除的雌性也具有生育能力。
结论
单独缺失Zfr2不足以导致小鼠雄性生育能力下降。
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