2019 AMMRA & AMPC Meeting
2019年 2月20日〜21日（Melbourne, Australia）
タイトル；Role of Vps52 during early mouse development.
（熊本大学 生命資源研究・支援センター 疾患モデル分野）
Previously, we identified Vps52 gene as a responsible gene for one of the t-complex recessive lethal mutations. Null mutation for Vps52 shows peri-implantation lethality at E6.5 resulted from the developmental defects in pluripotent epiblast, while Vps52 seems to be expressed in the visceral endoderm that is a cell layer surrounding epiblast and becomes a part of the yolk sac at later stage. Furthermore, epiblast specific Vps52 knockout embryos could survive until mid-gestation at E10.5, which support the hypothesis that Vps52 acts as a mediator of the cell-cell interaction between visceral endoderm and epiblast to regulate epiblast proliferation and differentiation.
It is known that VPS52 is a core component of the Golgi-associated retrograde protein (GARP) complex and interacts with VPS51, VPS53 and VPS54. The GARP complex is thought to be a tethering factor required for retrograde transport from endosomes to the trans-Golgi network, however, the function of the GARP complex as a regulator of mammalian development is still unclear. In this research, we analyzed phenotypes in mutant embryos for the components of the GARP complex and found that each mutant showed embryonic lethality but the phenotype was different among them. These results suggest that each component of GARP complex has different roles during mammalian early embryogenesis.