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Nat Commun. 2018 Oct 11;9(1):4217. doi: 10.1038/s41467-018-06738-5.

Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells.

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National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bellary Road, Bengaluru, 560065, India.
Institute for Bioengineering of Catalonia (IBEC), Barcelona, 08028, Spain.
University of Barcelona, Barcelona, 08036, Spain.
Raman Research Institute, C. V. Raman Avenue, Bengaluru, 560080, India.
Simons Centre for the Study of Living Machines, National Centre for Biological Sciences (NCBS), Bengaluru, 560065, India.
CSIR - Indian Institute of Integrative Medicine, Jammu, 180001, India.
Integrin Signalling Lab, Cell Biology & Physiology Program, Cell & Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, 28029, Spain.
University of Queensland, Institute for Molecular Bioscience and Centre for Microscopy and Microanalysis, St Lucia, QLD, 4072, Australia.
Department of Biochemistry, Weill Cornell Medical College, New York, NY, 10065, USA.
Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN) and Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, 08010, Spain.
National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bellary Road, Bengaluru, 560065, India.
Institute for Stem Cell Biology and Regenerative Medicine, Tata Institute of Fundamental Research (TIFR), Bengaluru, 560065, India.


Plasma membrane tension regulates many key cellular processes. It is modulated by, and can modulate, membrane trafficking. However, the cellular pathway(s) involved in this interplay is poorly understood. Here we find that, among a number of endocytic processes operating simultaneously at the cell surface, a dynamin independent pathway, the CLIC/GEEC (CG) pathway, is rapidly and specifically upregulated upon a sudden reduction of tension. Moreover, inhibition (activation) of the CG pathway results in lower (higher) membrane tension. However, alteration in membrane tension does not directly modulate CG endocytosis. This requires vinculin, a mechano-transducer recruited to focal adhesion in adherent cells. Vinculin acts by controlling the levels of a key regulator of the CG pathway, GBF1, at the plasma membrane. Thus, the CG pathway directly regulates membrane tension and is in turn controlled via a mechano-chemical feedback inhibition, potentially leading to homeostatic regulation of membrane tension in adherent cells.

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