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Quorum Sensing in the Plant Pathogen Erwinia carotovora subsp. carotovora: The Role of expREcc

April 2000 , Volume 13 , Number  4
Pages  384 - 393

Robert A. Andersson , 1 Anders R. B. Eriksson , 1 Riikka Heikinheimo , 1 Andres Mäe , 2 Minna Pirhonen , 1 Viia Kõiv , 2 Heidi Hyytiäinen , 3 Anne Tuikkala , 3 and E. Tapio Palva 3

1Department of Plant Biology, Uppsala Genetic Center, Swedish University of Agricultural Sciences, Box 7080, SE-75007, Uppsala, Sweden; 2Institute of Molecular and Cell Biology, Tartu University, 23 Riia Street, Tartu EE2400, Republic of Estonia; 3Department of Biosciences, Division of Genetics, and Institute of Biotechnology, Box 56, FIN-00014 University of Helsinki, Finland

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Accepted 4 January 2000.

The production of the main virulence determinants of the plant pathogen Erwinia carotovora subsp. carotovora, the extracellular cell wall-degrading enzymes, is partly controlled by the diffusible signal molecule N-(3-oxohexanoyl)-l-homoserine lactone (OHHL). OHHL is synthesized by the product of the expI/carI gene. Linked to expI we found a gene encoding a putative transcriptional regulator of the LuxR-family. This gene, expREcc, is transcribed convergently to the expI gene and the two open reading frames are partially overlapping. The ExpREcc protein showed extensive amino acid sequence similarity to the repressor EsaR from Pantoea stewartii subsp. stewartii(formerly Erwinia stewartii subsp. stewartii) and to the ExpREch protein of Erwinia chrysanthemi. Inactivation of the E. carotovora subsp. carotovora expREcc gene caused no decrease in virulence or production of virulence determinants in vitro. In contrast, there was a slight increase in the maceration capacity of the mutant strain. The effects of ExpREcc were probably mediated by changes in OHHL levels. Inactivation of expREcc resulted in increased OHHL levels during early logarithmic growth. In addition, over-expression of expREcc caused a clear decrease in the production of virulence determinants and part of this effect was likely to be caused by OHHL binding to ExpREcc. ExpREcc did not appear to exhibit transcriptional regulation of expI, but the effect on OHHL was apparently due to other mechanisms.

© 2000 The American Phytopathological Society