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Seminars and Colloquia


p120 ctn is a mechanotransducer that modulates E-Cadherin turnover by mechanical tension 
Fri, Dec 15, 2017,   03:00 PM to 04:00 PM at Seminar Room 34, 2nd Floor, Main Building

Dr. K. Venkatesan Iyer
Max Planck Institute for Molecular Cell Biology and Genetics.

Epithelial tissues comprise majority of tissues in our body and about 70-80 % of all cancers are of epithelial origin. These tissues are dynamically remodelled during growth and morphogenesis under the influence of morphogens and mechanical tension (MT). E-Cadherin – the primary cell-cell adhesion protein plays a crucial role in maintaining integrity and dynamic remodelling of epithelial tissues. But how MT, a key regulator of epithelial dynamics, influences the turnover of E-Cadherin is unknown. Here, we use in vivo model system of Drosophila pupal wing, a relatively flat tissue that generates MT during morphogenesis. Using cortical laser ablation and Fluorescence recovery after photobleaching (FRAP) techniques, we show that E-Cadherin turnover is strongly dependent on MT. By reducing tension in the pupal wing either by genetic perturbation or laser ablation we revealed that MT regulates E-Cadherin turnover. We show that mechano-regulation of E-Cadherin was mediated by modulation of endocytosis. Upon knocking down p120ctn, this mechano-regulation was abolished. Based on our findings, we propose that p120ctn is a novel mechanotransducer that modulates endocytosis of E-Cadherin by MT. Our results open new avenues towards understanding the role of p120ctn and E-Cadherin turnover in the link between tumour metastasis and its mechanical environment.