ArticlePloS one2015
Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 42 citations in OpenAlex.
- Deletion of exocyst component 5 suppresses repair of injured kidney by limiting cell proliferation.Cell death discovery · 2026Article
- Deficiency of exocyst complex component Exoc5 exacerbates the progression of kidney fibrosis.Experimental & molecular medicine · 2026Article
- The exocyst in ciliogenesis.Renal failure · 2025Review
- Sec10 suppresses antiviral innate immune response by facilitating STUB1-mediated STAT1 degradation.PLoS pathogens · 2025Article
- Ureter development and associated congenital anomalies.Nature reviews. Nephrology · 2025Review
- Sec10 negatively regulates antiviral immunity by downregulating NRF2-ATF4-RIG-I axis.International journal of biological sciences · 2025Article
- Oocyte-specific EXOC5 expression is required for mouse oogenesis and folliculogenesis.Molecular human reproduction · 2024Article
- Cilia-deficient renal tubule cells are primed for injury with mitochondrial defects and aberrant tryptophan metabolism.American journal of physiology. Renal physiology · 2024Article
- Null mutation of exocyst complex component 3-like does not affect vascular development in mice.Experimental animals · 2024Article
- The exocyst complex in neurological disorders.Human genetics · 2023Review
- Biallelic loss-of-function variants in EXOC6B are associated with impaired primary ciliogenesis and cause spondylo-epi-metaphyseal dysplasia with joint laxity type 3.Human mutation · 2022Review
- Exocyst inactivation in urothelial cells disrupts autophagy and activates non-canonical NF-κB signaling.Disease models & mechanisms · 2022Article
- Conditional Loss of the Exocyst Component Exoc5 in Retinal Pigment Epithelium (RPE) Results in RPE Dysfunction, Photoreceptor Cell Degeneration, and Decreased Visual Function.International journal of molecular sciences · 2021Article
- Article
- A genetic screen in Drosophila reveals an unexpected role for the KIP1 ubiquitination-promoting complex in male fertility.PLoS genetics · 2020Article
- Selenoprotein I is essential for murine embryogenesis.Archives of biochemistry and biophysics · 2020Article
- Roles for urothelium in normal and aberrant urinary tract development.Nature reviews. Urology · 2020Review
- Primary cilia and the exocyst are linked to urinary extracellular vesicle production and content.The Journal of biological chemistry · 2019Article
- The exocyst complex regulates insulin-stimulated glucose uptake of skeletal muscle cells.American journal of physiology. Endocrinology and metabolism · 2019Article
- Defects in the Exocyst-Cilia Machinery Cause Bicuspid Aortic Valve Disease and Aortic Stenosis.Circulation · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Most cases of congenital obstructive nephropathy are the result of ureteropelvic junction obstructions, and despite their high prevalence, we have a poor understanding of their etiology and scarcity of genetic models. The eight-protein exocyst complex regulates polarized exocytosis of intracellular vesicles in a large variety of cell types. Here we report generation of a conditional knockout mouse for Sec10, a central component of the exocyst, which is the first conditional allele for any exocyst gene. Inactivation of Sec10 in ureteric bud-derived cells using Ksp1.3-Cre mice resulted in severe bilateral hydronephrosis and complete anuria in newborns, with death occurring 6-14 hours after birth. Sec10 FL/FL;Ksp-Cre embryos developed ureteropelvic junction obstructions between E17.5 and E18.5 as a result of degeneration of the urothelium and subsequent overgrowth by surrounding mesenchymal cells. The urothelial cell layer that lines the urinary tract must maintain a hydrophobic luminal barrier again urine while remaining highly stretchable. This barrier is largely established by production of uroplakin proteins that are transported to the apical surface to establish large plaques. By E16.5, Sec10 FL/FL;Ksp-Cre ureter and pelvic urothelium showed decreased uroplakin-3 protein at the luminal surface, and complete absence of uroplakin-3 by E17.5. Affected urothelium at the UPJ showed irregular barriers that exposed the smooth muscle layer to urine, suggesting this may trigger the surrounding mesenchymal cells to overgrow the lumen. Findings from this novel mouse model show Sec10 is critical for the development of the urothelium in ureters, and provides experimental evidence that failure of this urothelial barrier may contribute to human congenital urinary tract obstructions.
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