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AlgT (sigma22) controls alginate production and tolerance to environmental stress in Pseudomonas syringae

Pseudomonas aeruginosa and the phytopathogen P. syringae produce the exopolysaccharide alginate, which is a copolymer of D-mannuronic and L-guluronic acids. One of the key regulatory genes controlling alginate biosynthesis in P. aeruginosa is algT, which encodes the alternate sigma factor, sigma(22)...

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Published in:Journal of bacteriology 1999-12, Vol.181 (23), p.7176-7184
Main Authors: Keith, L M, Bender, C L
Format: Article
Language:English
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Summary:Pseudomonas aeruginosa and the phytopathogen P. syringae produce the exopolysaccharide alginate, which is a copolymer of D-mannuronic and L-guluronic acids. One of the key regulatory genes controlling alginate biosynthesis in P. aeruginosa is algT, which encodes the alternate sigma factor, sigma(22). In the present study, the algT gene product from P. syringae pv. syringae showed 90% amino acid identity with its P. aeruginosa counterpart, and sequence analysis of the region flanking algT in P. syringae revealed the presence of nadB, mucA, and mucB in an arrangement virtually identical to that of P. aeruginosa. An algT mutant of P. syringae was defective in alginate production but could be complemented with wild-type algT from P. syringae or P. aeruginosa when expressed in trans. The algT mutant also displayed increased sensitivity to heat, paraquat, and hydrogen peroxide (H(2)O(2)); the latter two compounds are known to generate reactive oxygen intermediates. Signals for activation of algT gene expression in P. syringae were investigated with an algT::uidA transcriptional fusion. Like that in P. aeruginosa, algT transcription in P. syringae was activated by heat shock. However, algT expression in P. syringae was also stimulated by osmotic stress and by exposure to paraquat, H(2)O(2), and copper sulfate. The latter two compounds are frequently encountered during colonization of plant tissue and may be unique signals for algT activation in P. syringae.
ISSN:0021-9193
1098-5530
DOI:10.1128/jb.181.23.7176-7184.1999