By G. A. Beattie, S. E. Lindow (auth.), Jeffery L. Dangl (eds.)
The final decade has obvious an explosion in our figuring out of the way bacterial pathogens trick, cajole, usurp and parasitize their numerous hosts. This renaissance is because of the convergence of molecular and mobile innovations with the ability of microbial genetics. the aim of this quantity is to introduce fresh advances in realizing chosen platforms selected from either plant and animal hosts of bacterial pathogens. This slightly nonobvious collection of themes was once spurred through the new findings, exact by means of a number of conributors to this quantity, of universal structures used to secrete virulence elements from pathogens of either vegetation and animals. those serendipitous findings underscored the significance of simple learn techniques to parallel difficulties in biology. extra importantly, they introduced jointly investigators who won't have differently turn into conversant with each one other's experimental platforms. I, for one, locate the types of synergism mirrored in a quantity of this type to be essentially the most friendly elements of technological know-how and desire that the reader, even if a newcomer to the sector or a professional, can discover a new slant to outdated difficulties within the experiences contained h,E:lre. It was once, notwithstanding, essential to restrict quantity size, and this has pressured the exclusion of a few interesting bacterial pathosystems.
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Extra resources for Bacterial Pathogenesis of Plants and Animals: Molecular and Cellular Mechanisms
39 1 Introduction Xanthomonas campestris pathovar campestris (hereafter Xc. campestris) , the causal agent of black rot of crucifers, is a phytopathogenic bacterium of great economic importance (WILLIAMS 1980; ONSANDO 1992; SCHAAD and ALVAREZ 1993). Molecular genetic methods have now allowed a number of genes encoding pathogenicity determinants of Xc. campestris and related pathovars to be identified. In this chapter we will briefly review some of these and discuss our current understanding of the regulation of pathogenicity in this bacterium.
Campestris is also subject to coordinate negative regulation (TANG et al. 1990). Mutations in a gene designated rpfN give oveFproduction of the enzymes and xanthan, and, conversely overexpression of rpfN causes coordinate repression. rpfN encodes a protein of 46 KDa and is required for binding of a protein to sequences upstream of the promoter of the protease and endoglucanase structural genes. D. SOBY, B. J. DANIELS, in preparation). c. campestris contains a gene (clp) encoding a DNA-binding protein similar to the catabolite activation protein (CAP) of E.
J. Daniels pathogenesis. This can be tested by specific mutagenesis of the genes and subsequent plant assays. The choice of plant material for inoculation, the method of inoculation and levels of bacteria used undoubtedly influence the outcome of these pathogenicity tests in that different aspects of the disease process are probably being tested (SHAW and KADO 1988; DANIELS and LEACH 1993). In natural infections, Xc. campestris enters the plant principally through the hydathodes at the leaf margin, although secondary entry sites can develop in wounds or roots (COOK et al.
Bacterial Pathogenesis of Plants and Animals: Molecular and Cellular Mechanisms by G. A. Beattie, S. E. Lindow (auth.), Jeffery L. Dangl (eds.)
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