AI Article Synopsis
- Congenital urinary tract anomalies are common in infants and often linked to issues in ureter development, but the exact mechanisms behind this connection are not well understood.
- The gene Robo2 is crucial for normal ureter formation and its loss can lead to defects like vesicoureteral reflux, but its specific role in development has remained unclear until now.
- Research shows that ROBO2 interacts with retinaldehyde dehydrogenase-2 (RALDH2) to influence the migration and fusion of structures involved in ureter development, with potential treatments like retinoic acid offering hope for correcting these anomalies.
Article Abstract
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 Robo2embryo 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 Robo2embryo. These findings may be relevant to diverse disease conditions that are associated with altered signaling in the primitive bladder.
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| http://dx.doi.org/10.1016/j.ydbio.2020.06.002 | DOI Listing |
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