Coxsackie virus and adenovirus receptor (CXADR also known as CAR), a tight junction component molecule was reported to be expressed in epithelial cells. Previous studies reported that CXADR play an important role in tight junction complex. However, the role of CXDAR in blastocyst formation has not been investigated. Here we demonstrated that transcript levels of CXADR were elevated at eight-cell stage onward and highest at the blastocyst. To investigate the biological function of CXADR, we depleted both maternally and zygotically expressed CXADR employing an RNAi approach. Microinjection of CXADR siRNA resulted in a ~75% reduction of mRNA. In CXADR knockdown (KD) embryos, blastocyst development was significantly lower and most embryos were arrested at morula to blastocyst transition. We also found that genes required for and involved in tight junction biogenesis using qRT-PCR. Expression of tight junction component molecules including Cldn4, Ocln, and Tjp2 were decreased in the CXADR knock-down (KD) embryos. Moreover cell fate related genes such as Oct4, Cdx2, and Nanog were also downregulated in the KD embryos. In conclusion, our results suggested that CXADR affects establishment of tight junction complex and cell lineage in mouse blastocyst.
This work was supported by Next-Generation BioGreen21 Program (PJ 011213), Rural Development Administration (RDA), Republic of Korea.
20 Jul 2015 - 22 Jul 2015