Authors
Andrea Erlbruch, Alen Piljic, Charlotta Funaya, Zsófia Seboe-Lemke, Claude Antony, Carsten Schultz
Abstract
Cell wounding is commonly accompanied by a rupture of the plasma membrane. To protect cells against the sustained loss of cytoplasm and a pathological increase in [Ca2+]i, a rapid and effective repair machinery has to be activated to reseal the impact site. By live cell multiparamter imaging, we showed that after membrane damage, several Ca2+-effectors, such as annexins or PKC are recruited to the impact site in a highly spatiotemporally coordinated manner. We identified several annexins as components of the initial phase in the sealing process, but acting on the membranes independently and with different tasks. Corresponding with successful repair, annexin A4 was by far the fastest molecule to accumulate and to self-associate at the lesion,. Correlative electronmicroscopy revealed annexin A4 localization in the region of the impact. We conclude, that annexin A4 senses membrane damage, suggesting an important role in this pivotal cellular process.
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Aleksander Benjak
Scientific Officer | NCCR Molecular Systems Engineering, University of Basel
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