ArticleAmerican journal of physiology. Cell physiology2015
The exocyst gene Sec10 regulates renal epithelial monolayer homeostasis and apoptotic sensitivity.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- The exocyst in ciliogenesis.Renal failure · 2025Review
- A tale of Rabs and the exocyst complex in ciliary trafficking and biogenesis.Frontiers in cell and developmental biology · 2025Review
- 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
- The exocyst complex and intracellular vesicles mediate soluble protein trafficking to the primary cilium.Communications biology · 2024Article
- Exocyst controls exosome biogenesis via Rab11a.Molecular therapy. Nucleic acids · 2022Article
- MoSec61β, the beta subunit of Sec61, is involved in fungal development and pathogenicity, plant immunity, and ER-phagy inVirulence · 2020Article
- Review
- 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
- The role of the exocyst in renal ciliogenesis, cystogenesis, tubulogenesis, and development.Kidney research and clinical practice · 2019Review
- Article
- Exocyst Complex Member EXOC5 Is Required for Survival of Hair Cells and Spiral Ganglion Neurons and Maintenance of Hearing.Molecular neurobiology · 2018Article
- Regulation of Cell Polarity by Exocyst-Mediated Trafficking.Cold Spring Harbor perspectives in biology · 2018Review
- Routes and machinery of primary cilium biogenesis.Cellular and molecular life sciences : CMLS · 2017Review
- Arl13b and the exocyst interact synergistically in ciliogenesis.Molecular biology of the cell · 2016Article
- Emerging Insights into the Roles of Membrane Tethers from Analysis of Whole Organisms: The Tip of an Iceberg?Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The highly conserved exocyst protein complex regulates polarized exocytosis of subsets of secretory vesicles. A previous study reported that shRNA knockdown of an exocyst central subunit, Sec10 (Sec10-KD) in Madin-Darby canine kidney (MDCK) cells disrupted primary cilia assembly and 3D cyst formation. We used three-dimensional collagen cultures of MDCK cells to further investigate the mechanisms by which Sec10 and the exocyst regulate epithelial polarity, morphogenesis, and homeostasis. Sec10-KD cysts initially demonstrated undisturbed lumen formation although later displayed significantly fewer and shorter primary cilia than controls. Later in cystogenesis, control cells maintained normal homeostasis, while Sec10-KD cysts displayed numerous apoptotic cells extruded basally into the collagen matrix. Sec10-KD MDCK cells were also more sensitive to apoptotic triggers than controls. These phenotypes were reversed by restoring Sec10 expression with shRNA-resistant human Sec10. Apico-basal polarity appeared normal in Sec10-KD cysts, whereas mitotic spindle angles differed significantly from controls, suggesting a planar cell polarity defect. In addition, analysis of renal tubules in a newly generated kidney-specific Sec10-knockout mouse model revealed significant defects in primary cilia assembly and in the targeted renal tubules; abnormal epithelial cell extrusion was also observed, supporting our in vitro results. We hypothesize that, in Sec10-KD cells, the disrupted exocyst activity results in increased apoptotic sensitivity through defective primary cilia signaling and that, in combination with an increased basal cell extrusion rate, it affects epithelial barrier integrity and homeostasis.
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