Deciliation is associated with dramatic remodeling of epithelial cell junctions and surface domains. Export

@article{citeulike:3883779, abstract = {Stress-induced shedding of motile cilia (autotomy) has been documented in diverse organisms and likely represents a conserved cellular reaction. However, little is known about whether primary cilia are shed from mammalian epithelial cells and what impact deciliation has on polarized cellular organization. We show that several chemically distinct agents trigger autotomy in epithelial cells. Surprisingly, deciliation is associated with a significant, but reversible increase in transepithelial resistance. This reflects substantial reductions in tight junction proteins associated with "leaky" nephron segments (e.g., claudin-2). At the same time, apical trafficking of gp80/clusterin and gp114/CEACAM becomes randomized, basal-lateral delivery of Na,K-ATPase is reduced, and expression of the nonciliary apical protein gp135/podocalyxin is greatly decreased. However, ciliogenesis-impaired MDCK cells do not undergo continual junction remodeling, and mature cilia are not required for autotomy-associated remodeling events. Deciliation and epithelial remodeling may be mechanistically linked processes, because RNAi-mediated reduction of Exocyst subunit Sec6 inhibits ciliary shedding and specifically blocks deciliation-associated down-regulation of claudin-2 and gp135. We propose that ciliary autotomy represents a signaling pathway that impacts the organization and function of polarized epithelial cells.}, author = {Overgaard, C. E. and Sanzone, K. M. and Spiczka, K. S. and Sheff, D. R. and Sandra, A. and Yeaman, C.}, citeulike-article-id = {3883779}, citeulike-linkout-0 = {http://dx.doi.org/10.1091/mbc.E08-07-0741}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19005211}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19005211}, doi = {10.1091/mbc.E08-07-0741}, issn = {1939-4586}, journal = {Molecular biology of the cell}, keywords = {arl3, cilia, golgi}, month = {January}, number = {1}, pages = {102--113}, posted-at = {2009-01-13 21:50:34}, priority = {2}, title = {Deciliation is associated with dramatic remodeling of epithelial cell junctions and surface domains.}, url = {http://dx.doi.org/10.1091/mbc.E08-07-0741}, volume = {20}, year = {2009} }

TY - JOUR ID - citeulike:3883779 L3 - citeulike-article-id:3883779 N2 - Stress-induced shedding of motile cilia (autotomy) has been documented in diverse organisms and likely represents a conserved cellular reaction. However, little is known about whether primary cilia are shed from mammalian epithelial cells and what impact deciliation has on polarized cellular organization. We show that several chemically distinct agents trigger autotomy in epithelial cells. Surprisingly, deciliation is associated with a significant, but reversible increase in transepithelial resistance. This reflects substantial reductions in tight junction proteins associated with "leaky" nephron segments (e.g., claudin-2). At the same time, apical trafficking of gp80/clusterin and gp114/CEACAM becomes randomized, basal-lateral delivery of Na,K-ATPase is reduced, and expression of the nonciliary apical protein gp135/podocalyxin is greatly decreased. However, ciliogenesis-impaired MDCK cells do not undergo continual junction remodeling, and mature cilia are not required for autotomy-associated remodeling events. Deciliation and epithelial remodeling may be mechanistically linked processes, because RNAi-mediated reduction of Exocyst subunit Sec6 inhibits ciliary shedding and specifically blocks deciliation-associated down-regulation of claudin-2 and gp135. We propose that ciliary autotomy represents a signaling pathway that impacts the organization and function of polarized epithelial cells. IS - 1 JF - Molecular biology of the cell SN - 1939-4586 EP - 113 TI - Deciliation is associated with dramatic remodeling of epithelial cell junctions and surface domains. VL - 20 SP - 102 KW - arl3 KW - cilia KW - golgi AU - Overgaard, CE AU - Sanzone, KM AU - Spiczka, KS AU - Sheff, DR AU - Sandra, A AU - Yeaman, C PY - 2009/01// UR - http://dx.doi.org/10.1091/mbc.E08-07-0741 ER -