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First published online October 22, 2008
doi: 10.1242/10.1242/jcs.032169
Research Article |
1 Section of Membrane Biology, Laboratory of Cellular and Molecular Biophysics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892-1855, USA
2 Department of Biology, Technion-Israel Institute of Technology, Haifa, 32000 Israel
3 Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel
* Author for correspondence (e-mail: chernoml{at}mail.nih.gov)
Accepted 5 August 2008
Cell-cell fusion in animal development and in pathophysiology involves expansion of nascent fusion pores formed by protein fusogens to yield an open lumen of cell-size diameter. Here we explored the enlargement of micron-scale pores in syncytium formation, which was initiated by a well-characterized fusogen baculovirus gp64. Radial expansion of a single or, more often, of multiple fusion pores proceeds without loss of membrane material in the tight contact zone. Pore growth requires cell metabolism and is accompanied by a local disassembly of the actin cortex under the pores. Effects of actin-modifying agents indicate that the actin cortex slows down pore expansion. We propose that the growth of the strongly bent fusion-pore rim is restricted by a dynamic resistance of the actin network and driven by membrane-bending proteins that are involved in the generation of highly curved intracellular membrane compartments.
Key words: Cell fusion, Syncytium formation, Fusion-pore expansion, Actin cytoskeleton, Membrane-bending proteins, Baculovirus gp64
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