Lesson plan
Tabtoxin
Tabtoxin, also known as wildfire toxin, is a monobactam-type phytotoxin produced by Pseudomonas syringae. It is the precursor to the antibiotic tabtoxinine β-lactam (TBL). It is produced by: * Pseudomonas syringae pv. tabaci, the causal agent of the wildfire of tobacco * P. syringae pv. coronafaciens * P. syringae pv. garcae * P. syringae BR2, which causes a disease of bean (Phaseolus vulgaris) similar to tobacco wildfire. This organism is closely related to P. syringae pv. tabaci but cannot be classified in the pathovar tabaci because it is not pathogenic on tobacco. Tabtoxin is a dipeptide precursor to the biologically active form of TBL, differing by having an extra threonine attached by a peptide bond to the C terminus. Tabtoxin is required by BR2(R) for both chlorosis and lesion formation on bean. All mutations that affected tabtoxin production, whether spontaneous deletion or transposon-induced, also affected lesion formation, and in all cases, restoration of tabtoxin production also restored pathogenic symptoms. Other factors may be required for BR2 to be pathogenic on bean, but apparently these are in addition to tabtoxin production. This toxin is a irreversible inhibitor of glutamine synthetase.
Article summary
Tabtoxin, also known as wildfire toxin, is a monobactam-type phytotoxin produced by Pseudomonas syringae. It is the precursor to the antibiotic tabtoxinine β-lactam (TBL). It is produced by: * Pseudomonas syringae pv. tabaci, the causal agent of the wildfire of tobacco * P. syringae pv. coronafaciens * P. syringae pv. garcae * P. syringae BR2, which causes a disease of bean (Phaseolus vulgaris) similar to tobacco wildfire. This organism is closely related to P. syringae pv. tabaci but cannot be classified in the pathovar tabaci because it is not pathogenic on tobacco. Tabtoxin is a dipeptide precursor to the biologically active form of TBL, differing by having an extra threonine attached by a peptide bond to the C terminus. Tabtoxin is required by BR2(R) for both chlorosis and lesion formation on bean. All mutations that affected tabtoxin production, whether spontaneous deletion or transposon-induced, also affected lesion formation, and in all cases, restoration of tabtoxin production also restored pathogenic symptoms. Other factors may be required for BR2 to be pathogenic on bean, but apparently these are in addition to tabtoxin production. This toxin is a irreversible inhibitor of glutamine synthetase.
Key claims
No claims recorded.
Discussion questions
- Summarise the article in your own words. Which single claim would you verify first, and why?
- Which claim in this article is most likely to be revised as the sources update? How would you check its current status?
- If two sources disagreed about one of these facts, what would you need in order to trust one over the other?
Bibliography
No sources recorded.
Key claims and bibliography are generated from the same tracked claims and sources as the article page.