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Uterine Rbpj is required for embryonic-uterine orientation and decidual remodeling via Notch pathway-independent and -dependent mechanisms.

  • Author(s): Zhang, Shuang
  • Kong, Shuangbo
  • Wang, Bingyan
  • Cheng, Xiaohong
  • Chen, Yongjie
  • Wu, Weiwei
  • Wang, Qiang
  • Shi, Junchao
  • Zhang, Ying
  • Wang, Shumin
  • Lu, Jinhua
  • Lydon, John P
  • DeMayo, Francesco
  • Pear, Warren S
  • Han, Hua
  • Lin, Haiyan
  • Li, Lei
  • Wang, Hongmei
  • Wang, Yan-Ling
  • Li, Bing
  • Chen, Qi
  • Duan, Enkui
  • Wang, Haibin
  • et al.
Abstract

Coordinated uterine-embryonic axis formation and decidual remodeling are hallmarks of mammalian post-implantation embryo development. Embryonic-uterine orientation is determined at initial implantation and synchronized with decidual development. However, the molecular mechanisms controlling these events remain elusive despite its discovery a long time ago. In the present study, we found that uterine-specific deletion of Rbpj, the nuclear transducer of Notch signaling, resulted in abnormal embryonic-uterine orientation and decidual patterning at post-implantation stages, leading to substantial embryo loss. We further revealed that prior to embryo attachment, Rbpj confers on-time uterine lumen shape transformation via physically interacting with uterine estrogen receptor (ERα) in a Notch pathway-independent manner, which is essential for the initial establishment of embryo orientation in alignment with uterine axis. While at post-implantation stages, Rbpj directly regulates the expression of uterine matrix metalloproteinase in a Notch pathway-dependent manner, which is required for normal post-implantation decidual remodeling. These results demonstrate that uterine Rbpj is essential for normal embryo development via instructing the initial embryonic-uterine orientation and ensuring normal decidual patterning in a stage-specific manner. Our data also substantiate the concept that normal mammalian embryonic-uterine orientation requires proper guidance from developmentally controlled uterine signaling.

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