Transgene-mediated rescue of spermatogenesis in Cldn11-null mice.
Transgene-mediated rescue of spermatogenesis in Cldn11-null mice.
复制标题
转基因介导的 Cldn11 缺失小鼠精子发生的拯救。
DOI：
10.1095/biolreprod.111.096230
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发表时间：
2012
影响因子：
3.6
通讯作者：
Gow,Alexander
中科院分区：
文献类型：
--
作者：
Wu,Xin;Peppi,Marcello;Vengalil,MatthewJ;Maheras,KathleenJ;Southwood,CherieM;Bradley,Michael;Gow,Alexander
Claudins comprise a large family of tight junction (TJ) proteins that are often expressed broadly during development and in adult tissues and constitute the physical barriers that occlude the paracellular space in polarized epithelia. In mouse testis, the integrity of TJs is critical to normal spermatogenesis and is dependent on CLDN11 expression. In the current study, we have generated multiple transgenic mouse lines in which steady-state levels of transgene-derivedCldn11mRNA are up to fourfold greater than endogenous gene expression. Spermatogenesis in all founder mice harboring two copies of the endogenousCldn11gene is normal. These animals breed well, indicating that transgene overexpression, at least at the level of mRNA, is well tolerated by Sertoli cells. In addition, we demonstrate that the promoter/enhancer of the transgene, comprising 5 kb of genomic sequence upstream of exon 1 of the mouseCldn11gene, is sufficient to rescue azoospermia inCldn11-null mice. Finally, using transient transgenic mice, we narrow the location of Sertoli cell-specificcisregulatory elements to a 2-kb region upstream of theCldn11transcription start site. Together, these data provide essential information for further investigation of the biological regulation of CLDN11 TJs in the testis.
