Clostridium botulinum

 Botulinum neurotoxin serotype A (BoNT/A) has achieved a dichotomous status in modern medicine; it is both a versatile treatment for several neurological disorders and a lethal poison responsible for causing the neuroparalytic syndrome botulism.

 The extent of paralysis largely depends on the dosage of toxin received. The toxins block neurotransmitter release by delivering their Zn(2+)-dependent protease components to the presynaptic side of chemical synapses.

 These highly specialized enzymes exclusively hydrolyze peptide bonds within SNARE (soluble N-ethylmaleiamide-sensitive factor attachment protein receptor) proteins.

 The structural basis for the highly specific interaction between BoNT/A and its target SNARE, SNAP-25 (synaptosomal-associated protein of 25kDa), is now elucidated.

References

 Breidenbach MA, Brunger AT. New insights into clostridial neurotoxin-SNARE interactions. Trends Mol Med. 2005 Aug;11(8):377-81. PMID: 16006188