Abstract

Growth of Sinorhizobium meliloti under Pi-limiting conditions induced expression of the major H2O2-inducible catalase (HPII) gene (katA) in this organism. This transcription required the PhoB transcriptional regulator and initiated from a promoter that was distinct from the OxyR-dependent promoter which activates katA transcription in response to addition of H2O2. In N2-fixing root nodules, katA was transcribed from the OxyR- and not the PhoB-dependent promoter. This is consistent with the accumulation of reactive oxygen species (ROS) in nodules and also indicates that bacteroids within nodules are not Pi-limited. Pi-limited growth also induced expression of catalase genes in Agrobacterium tumefaciens (HPI) and Pseudomonas aeruginosa (PA4236-HPI) suggesting that this may be a widespread phenomenon. The response is not a general stress response as in both S. meliloti and P. aeruginosa increased transcription is mediated by the phosphate responsive transcriptional activator PhoB. The phenotypic consequences of this response were demonstrated in S. meliloti by the dramatic increase in H2O2 resistance of wild type but not phoB mutant cells upon growth in Pi-limiting media. Our data indicate that in S. meliloti, katA and other genes whose products are involved in protection from oxidative stress are induced upon Pi-limitation. These observations suggest that as part of the response to Pi-limitation, S. meliloti, P. aeruginosa and A. tumefaciens have evolved a capacity to increase their resistance to oxidative stress. Whether this capacity evolved because Pi-starved cells generate more ROS or whether the physiological changes that occur in the cells in response to Pi-starvation render them more sensitive to ROS remains to be established.

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