Transcriptional regulation by iron and role during plant pathogenesis of genes encoding iron- and manganese-superoxide dismutases of Pseudomonas syringae pv. syringae B728a

Citation
Yc. Kim et al., Transcriptional regulation by iron and role during plant pathogenesis of genes encoding iron- and manganese-superoxide dismutases of Pseudomonas syringae pv. syringae B728a, PHYSL MOL P, 55(6), 1999, pp. 327-339
Citations number
62
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PHYSIOLOGICAL AND MOLECULAR PLANT PATHOLOGY
ISSN journal
08855765 → ACNP
Volume
55
Issue
6
Year of publication
1999
Pages
327 - 339
Database
ISI
SICI code
0885-5765(199912)55:6<327:TRBIAR>2.0.ZU;2-1
Abstract
The bean pathogen, Pseudomonas syringae B728a, may require iron-superoxide dismutase (FeSOD) and manganese-superoxide dismutase (MnSOD) activity in pr otection against reactive oxygen species (ROS) generated in planta. Genes e ncoding FeSOD or MnSOD of P. syringae B728a were cloned by hybridization wi th specific PCR probes amplified from P. syringaa genomic DNA. The sodB gen e was monocistronic whereas the sodA gene was transcribed as part of a 1.4 kb polycistronic operon, consisting of orfX-sodA. A putative Fur consensus sequence was located upstream of the orf-sodA operon. The sodB (FeSOD) gene was expressed throughout growth, but was down regulated under iron deficie nt conditions. In contrast, the sodA (MnSOD) gene was expressed only under iron deficient conditions. Mutants defective in sodA and sodB genes were ge nerated by marker exchange mutagenesis. Unlike other bacterial SOD deficien t mutants, the P. syringae B728a sodAsodB mutant was not impaired in growth on rich or minimal medium, but it was more sensitive to paraquat than wild -type. The P. syringae B728a SOD deficient mutants caused bacterial brown s pot disease on bean pods or leaves to the same extent as wild-type. Thus, t hese superoxide dismutases may not be key enzymes for aerobic metabolism an d pathogenicity in P. syringae B728a. (C) 1999 Academic Press.