Li Minyan, Huang Rui, Jiang Xue, Chen Yuxi, Zhang Zhen, Zhang Xiya, Liang Puping, Zhan Shaoquan, Cao Shanbo, Songyang Zhou, Huang Junjiu
Guangdong Province Key Laboratory of Reproductive Medicine, School of Life Sciences and the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
State Key Laboratory of Biocontrol, Institute of Healthy Aging Research and SYSU-BCM Joint Research Center, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
PLoS One. 2015 Nov 24;10(11):e0143148. doi: 10.1371/journal.pone.0143148. eCollection 2015.
Mammalian spermatogenesis is a highly regulated multistage process of sperm generation. It is hard to uncover the real function of a testis specific gene in vitro since the in vitro model is not yet mature. With the development of the CRISPR/Cas9 (Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR-associated 9) system, we can now rapidly generate knockout mouse models of testis specific genes to study the process of spermatogenesis in vivo. SYCP3-like X-linked 2 (SLX2) is a germ cell specific component, which contains a Cor1 domain and belongs to the XLR (X-linked, lymphocyte regulated) family. Previous studies suggested that SLX2 might play an important role in mouse spermatogenesis based on its subcellular localization and interacting proteins. However, the function of SLX2 in vivo is still elusive. Here, to investigate the functions of SLX2 in spermatogenesis, we disrupted the Slx2 gene by using the CRISPR/Cas9 system. Since Slx2 is a testis specific X-linked gene, we obtained knockout male mice in the first generation and accelerated the study process. Compared with wild-type mice, Slx2 knockout mice have normal testis and epididymis. Histological observation of testes sections showed that Slx2 knockout affected none of the three main stages of spermatogenesis: mitosis, meiosis and spermiogenesis. In addition, we further confirmed that disruption of Slx2 did not affect the number of spermatogonial stem cells, meiosis progression or XY body formation by immunofluorescence analysis. As spermatogenesis was normal in Slx2 knockout mice, these mice were fertile. Taken together, we showed that Slx2 itself is not an essential gene for mouse spermatogenesis and CRISPR/Cas9 technique could speed up the functional study of testis specific X-linked gene in vivo.
哺乳动物精子发生是一个受到高度调控的精子生成多阶段过程。由于体外模型尚未成熟,很难在体外揭示睾丸特异性基因的真正功能。随着CRISPR/Cas9(成簇规律间隔短回文重复序列/CRISPR相关蛋白9)系统的发展,我们现在可以快速生成睾丸特异性基因的敲除小鼠模型,以研究体内精子发生过程。类SYCP3 X连锁蛋白2(SLX2)是一种生殖细胞特异性成分,它含有一个Cor1结构域,属于XLR(X连锁、淋巴细胞调节)家族。先前的研究表明,基于其亚细胞定位和相互作用蛋白,SLX2可能在小鼠精子发生中发挥重要作用。然而,SLX2在体内的功能仍然不清楚。在这里,为了研究SLX2在精子发生中的功能,我们使用CRISPR/Cas9系统破坏了Slx2基因。由于Slx2是一个睾丸特异性X连锁基因,我们在第一代就获得了敲除雄性小鼠,加快了研究进程。与野生型小鼠相比,Slx2敲除小鼠的睾丸和附睾正常。睾丸切片的组织学观察表明,Slx2敲除不影响精子发生的三个主要阶段:有丝分裂、减数分裂和精子形成。此外,我们通过免疫荧光分析进一步证实,Slx2的破坏不影响精原干细胞的数量、减数分裂进程或XY小体的形成。由于Slx2敲除小鼠的精子发生正常,这些小鼠是可育的。综上所述,我们表明Slx2本身不是小鼠精子发生的必需基因,并且CRISPR/Cas9技术可以加快体内睾丸特异性X连锁基因的功能研究。