Abstract
Permeabilization of the plasma membrane represents an important threat for any cell, since it compromises its viability by disrupting cell homeostasis. Numerous pathogenic bacteria produce pore-forming toxins that break plasma membrane integrity and cause cell death by colloid-osmotic lysis. Eukaryotic cells, in turn, have developed different ways to cope with the effects of such membrane piercing. Here, we provide a short overview of the general mechanisms currently proposed for plasma membrane repair, focusing more specifically on the cellular responses to membrane permeabilization by pore-forming toxins and presenting new data on the effects and cellular responses to the permeabilization by an RTX (repeats in toxin) toxin, the adenylate cyclase toxin-hemolysin secreted by the whooping cough bacterium Bordetella pertussis, which we have studied in the laboratory.
Highlights
The plasma membrane, a thin layer of only ≈40 Å thickness, regulates the necessary flow of matter, energy, and information between the cell interior and the external medium for cells to live, and its structural integrity is essential for the proper functioning of cells
Despite it was reported previously that wounded eukaryotic cells repair more or less large wounds in their plasma membrane in a few seconds, by a mechanism strictly dependent on extracellular Ca2+ [1,2], a systematic study of plasma membrane repair was not developed till the 1990s, with the works of McNeil and Steinhardt [3], who demonstrated that Ca2+ entry into wounded cells triggers exocytosis of intracellular vesicles close to the wound site [4,5]
It was clear that plasma membrane repair represents an active, energy-dependent process that is orchestrated by specific membrane traffic events [6]
Summary
The plasma membrane, a thin layer of only ≈40 Å thickness, regulates the necessary flow of matter, energy, and information between the cell interior and the external medium for cells to live, and its structural integrity is essential for the proper functioning of cells. Wounds due to mechanical scratching are not delimited by protein boundaries and have an proteins give rise to holes with defined boundaries (“proteinaceous or proteolipidic pores”) (Figure exclusively lipidic lumen (“lipid pores”), while membrane damage by pore-forming proteins give rise. Within damage limits [13] and will in turn be influenced by the lipid composition of the membrane pore-forming proteins create stable holes that do not close spontaneously, and an energy cost paid by [14]. Toroidal pores differ from the more classical purely proteinaceous pores in that: (i) the pore characteristics depend on the membrane lipid composition, (ii) they have lower stability than pure proteinaceous pores, and (iii) the pore size may vary with the protein concentration and the incubation time [15,16].
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