Rapalog-induced cell adhesion molecule inhibits mesoderm migration in Xenopus embryos by increasing frequency of adhesion to the ectoderm

During the gastrula stage of Xenopus laevis, mesodermal cells migrate on the blastocoel roof (BCR) toward the animal pole. In this process, mesodermal cells directly adhere to the BCR via adhesion molecules, such as cadherins, which in turn trigger a repulsive reaction through factors such as Eph/ephrin. Therefore, the mesoderm and BCR repeatedly adhere to and detach from each other, and the frequency of this adhesion is thought to control mesoderm migration. Although knockdown of cadherin or Eph/ephrin causes severe gastrulation defects, these molecules have been reported to contribute not only to boundary formation but also to the internal function of each tissue. Therefore, it is possible that the defect caused by knockdown occurs due to tissue function abnormalities. To address this problem, we developed a method to specifically induce adhesion between different tissues using rapalog (an analog of rapamycin). When adhesion between the BCR and mesoderm was specifically enhanced by rapalog, mesoderm migration was strongly suppressed. Furthermore, we confirmed that rapalog significantly increased the frequency of adhesion between the two tissues. These results support the idea that the adhesion frequency controls mesoderm migration, and demonstrate that our method effectively enhances adhesion between specific tissues in vivo.

Automated summary

During the gastrula stage of Xenopus laevis, the adhesion frequency between the blastocoel roof and mesodermal cells is found to control mesoderm migration. Enhancing adhesion between these tissues effectively suppresses mesoderm migration.