Genetics of Phytopathogenic Bacteria
Only a small proportion of bacteria are plant pathogenic and have developed mechanisms to invade and colonize their host plants and cause disease. However, resistant host-plant cultivars and certain non-host plants are able to recognize and combat phytopathogenic bacteria. These resistant plants react with a localized induced cell death at the site of infection; this is termed hypersensitive response (HR) and is induced by so-called elicitors, such as avirulence proteins (Avr proteins). These are recognized by corresponding receptor proteins in the plant. It has been shown that the ability to cause disease in compatible interactions with host plants and the induction of HR in incompatible interactions both depend on the ability of the bacteria to express a cluster of genes termed hrp. (hypersensitive reaction and pathogenicity; Lindgren et al. 1986). Thus, hrp. mutants of plant pathogenic bacteria cause no detectable reactions in either host or non-host plants. Hrp genes seem to be a common feature of all Gram-negative plant pathogenic bacteria. Some of the hrp. genes encode a protein-secretion mechanism known from animal pathogenic bacteria (the type III secretion system) which apparently enables them to direct proteins into plant cells. The type III secretion system differs markedly from the earlier discovered type I protein secretion [which involves adenosine triphosphate (ATP)-binding cassette transporters] and the signal-peptide/sec-dependent type II secretion system (Salmond and Reeves 1993; Lee 1997).
KeywordsHypersensitive Response Secretion System Xanthomonas Campestris Plant Pathogenic Bacterium Phytopathogenic Bacterium
Unable to display preview. Download preview PDF.
- Alfano JR, Bauer TM, Milos TM, Collmer A (1996) Analysis of the role of the Pseudomonas syringa. pv. syringa. HrpZ harpin in elicitation of the hypersensitive response in tobacco using functionally non-polar hrp. deletion mutations, truncated HrpZ fragments, and hrm. mutations. Mol Microbiol 19:715–728PubMedCrossRefGoogle Scholar
- Charkowski AO, Huang HC, Collmer A (1997) Altered localization of HrpZ in Pseudomonas syringa. pv. syringae hr. mutants suggests that different components of the type III secretion pathway control protein translocation across the inner and outer membranes of Gram-negative bacteria. J Bacteriol 197:3866–3874Google Scholar
- Dietrich RA, Delaney TP, Uknes SJ, Ward EJ, Ryales JA, Dangl JL (1994) Arabidopsi. mutants simulating disease resistance response. Cell 77:565–578Google Scholar
- Engelbrecht F, Dominguez-Bernal G, Hess J, Dickneite C, Greiffenberg L, Lampidis R, Raffelsbauer D, Daniels JJ, Kreft J, Kaufmann SH, Vazques-Boland JA, Goebel W (1998) A novel PrfA-regulated chromosomal locus, which is specific for Listeria ivanovi., encodes two small, secreted internalins and contributes to virulence in mice. Mol Microbiol 30:405–417PubMedCrossRefGoogle Scholar
- Gopolan S, Bauer DW, Alfano JR, Loniello AO, He SY, Collmer A (1996) Expression of the Pseudomonas syringa. avirulence protein AvrB in plant cells alleviates its dependence on the hypersensitive response and pathogenicity (Hrp) secretion system in eliciting genotype specific hypersensitive cell death. Plant Cell 9:1095–1105Google Scholar
- Hammond-Kosak KE, Jones JDG (1996) Resistance gene-dependent plant defence responses. Plant Cell 8:1776–1791Google Scholar
- Huang HC, Schurik R, Denny TP, Atkinson MM, Baker Cj, Yucel I, Hutcheson SW, Collmer A (1988) Molecular cloning of a Pseudomonas syringa. pv. syringa. gene cluster that enables Pseudomonas fluorescen. to elicit the hypersensitive response in tobacco plants. J Bacteriol 170:4748–4756PubMedGoogle Scholar
- Rosquist DE, Magnusson K-E, Wolf-Watz H (1994) Target cell contact triggers expression and polarized transfer of the Yersini. YopE cytotoxin into mammalian cells. EMBO J 13:964–972Google Scholar
- Sory MP, Boland A, Lambermont I, Cornelis GR (1995) Identification of the YopE and YopH domains required for secretion and internalization into the cytosol of macrophages, using the cya. gene fusion approach. Proc Natl Acad Sci USA 92:11998–112002Google Scholar