Kurzfassung

Membrane pore forming proteins are employed by species of all kingdoms to attack target cells. Pore forming toxins (PFTs) represent the largest group of known protein toxins produced by bacteria. Several structural families of PFTs are recognized today, with beta-PFTs being the best characterized and largest group. Membrane pores lead to uncontrolled flux of ions and water, which may ultimately lead to cell death. Yet, cells are not inevitably killed by PFTs, but have evolved mechanisms which...Membrane pore forming proteins are employed by species of all kingdoms to attack target cells. Pore forming toxins (PFTs) represent the largest group of known protein toxins produced by bacteria. Several structural families of PFTs are recognized today, with beta-PFTs being the best characterized and largest group. Membrane pores lead to uncontrolled flux of ions and water, which may ultimately lead to cell death. Yet, cells are not inevitably killed by PFTs, but have evolved mechanisms which enable them to survive a limited number of lesions. One aim of our studies is to elucidate these mechanisms. Recently, we found that calcium influx dependent repair (CIDER), default mechanism for the repair of large membrane lesions, also operates in the case of a newly discovered small b-PFT featuring pores permissive for calcium ions. In contrast, other small beta-PFTs appear to not permit rapid influx of calcium ions, thus allowing for subversion of repair (SORE). Ongoing research aims at deciphering the mechanisms of membrane repair and microbial strategies to subvert them.
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