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Similarly, this technique has been used to characterize the dissemination patterns of various B. anthracis mutant strains deficient in one or more toxin components (Loving et al., 2009).
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Lethal toxin isogenic mutant bacteria lacks single toxin components and is therefore greatly attenuated [6] [7].
Although cardiac defects triggered by anthrax toxin seem to depend upon the presence of two toxin components, i.e., lethal toxin (PA+LF) and edema toxin (PA+EF) [1], the two toxins apparently affect cardiac function using distinct mechanisms.
These three toxin components combine to form two binary toxins, lethal toxin (LT), a zinc metalloprotease that cleaves mitogen activated protein kinases [8], and edema toxin (ET), an adenylate cyclase that increases intracellular cyclic AMP concentrations [9].
Immediately prior to injection, toxin components were thawed and mixed in PBS.
The observed cardiovascular defects induced by anthrax toxins were dependent on the presence of two toxin components (PA+LF or PA+EF).
All these toxins consist of two separate toxin components.
It should be noted that some toxin components of the toxin antitoxin system have RNase activities [ 30].
One isolate did not have any toxin gene, 4 isolates carried one toxin gene (seq), and 87 isolates had two or more toxin genes.
However, the MazF toxin component of MazEF modules appeared to be more prevalent in human gut metagenomes than the corresponding antitoxin or other TA genes, and this was also the case in the marine and murine metagenomes (Fig 3c).
Moreover, the results obtained from a principal component analysis (PCA) showed that the "bad bugs" had surprisingly more toxin-antitoxin modules than did the controls.
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