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首页> 外文期刊>Journal of Clinical Microbiology >Further characterization of proteolytic Clostridium botulinum type A5 reveals that neurotoxin formation is unaffected by loss of the cntR (botR) promoter sigma factor binding site.
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Further characterization of proteolytic Clostridium botulinum type A5 reveals that neurotoxin formation is unaffected by loss of the cntR (botR) promoter sigma factor binding site.

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Although widely recognized as forming a deadly food-borne intoxicant, proteolytic Clostridium botulinum also infects humans, causing infant botulism after growth and neurotoxin formation in the gut (1) and wound botulism after contamination of a wound, often following injected drug abuse (8). The genes encoding the neurotoxin and its accessory proteins form two operons whose expression is induced by CntR (BotR), an alternative sigma factor (5). Comparative genomics of proteolytic C. botulinum recently identified four wound botulism strains as being closely related, each carrying identical copies of a new subtype (A5) of the A neurotoxin gene (3).

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