Correlation Engine 2.0
Clear Search sequence regions

  • aldehyde (2)
  • apoptosis (1)
  • bladder (6)
  • mice (1)
  • mice knockout (1)
  • RALDH2 (3)
  • receptors (2)
  • reflux (1)
  • ROBO2 (8)
  • signal (1)
  • ureter (8)
  • Sizes of these terms reflect their relevance to your search.

    Congenital anomalies of the urinary tract are a significant cause of morbidity in infancy, and many congenital anomalies are linked to ureter development; however, the mechanism by which congenital anomalies control ureter development remains unknown. The loss of Robo2 can cause ureter defects and vesicoureteral reflux. However, how Robo2 impacts ureter development is unclear. We found that ROBO2 is expressed in the common nephric duct (CND) and primitive bladder, and impacts CND migration and fusion with the primitive bladder via its novel binding partner retinaldehyde dehydrogenase-2 (RALDH2). Delayed apoptosis that is due to the failure of CND fusion with the primitive bladder in the Robo2-/-embryo results in an abnormal ureter connection to the CND, which is required for ureter development. We define a novel pathway in which the CND is remodeled by ROBO2 and retinoic acid rescued the ureter anomalies in the Robo2-/-embryo. These findings may be relevant to diverse disease conditions that are associated with altered signaling in the primitive bladder. Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.


    Qinggang Li, Jiayao Ji, Shaoyuan Cui, Ying Liu, Qian Ma, Bo Fu, Jurong Yang, Yunming Xiao, Xueyuan Bai, Guanyan Cai, Yuansheng Xie, Xiangmei Chen. ROBO2-mediated RALDH2 signaling is required for common nephric duct fusion with primitive bladder. Developmental biology. 2020 Aug 15;464(2):103-110

    Expand section icon Mesh Tags

    Expand section icon Substances

    PMID: 32562756

    View Full Text