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e regulatory proteins that control the expression of T3SS upon host infection, structure proteins that build the needle complex, effectors that are secreted and are responsible for the virulence and chaperones that help with the secretion of effectors (Buttner and He, 2009).

 

The expression of T3SS genes is coordinately regulated by many endogenous regulatory proteins and various external environmental factors (Rahme et al. 1992; Xiao et al. 1992). Multiple signal transduction components have been identified in the gene regulation pathways. The mechanism of regulation is highly variable from mammalian pathogens to plant bugs. Most T3SSs in animal pathogens are activated after the bacteria contact with the surface of eukaryotic cells (Hueck, 1998). For example, before cell contact, the channels of Yersinia spp.T3SS are shut by an outer membrane protein YopN, and a negative transcription factor LcrQ that represses yop (Yersinia outer protein) genes. Upon cell contact, YopN is removed, resulting in secretion of LcrQ, which in turn releases the repression of yop genes (Rosqvist et al. 1994). The mechanisms of T3SS gene regulation in the plant bacterial pathogens are divided into two main groups. The hrp genes of Pseudomonas syringae, Erwinia spp. and Pantoea stewartii belong to group I that is regulated by the HrpL, an ECF (extracytoplasmic factor) family alternate sigma factor. On the other hand, the hrp genes in group II are activated by an AraC-like activator, such as HrpX in Xanthomonas spp. and HrpB in Ralstonia solanacearum (Alfano and Collmer 1997).hrp genes are expressed at a very low level in the nutrient rich medium, but activated in the hrp-inducing minimal medium, which is believed to largely mimic the plant apoplast conditions (Jin et al. 2003). The details of the mechanisms that the phytopathogenic bacteria use to activate T3SS are discussed in the following sections.

 

As soon as the expression of T3 genes is activated, the needle-like T3SS apparatus is constructed. In Pseudomonas syringae, the basal body of the T3SS is encoded by the so-called hrc (hypersensitive response and conserved) genes, which are highly conserved between diverse plant and animal pathogens (Collmer et al. 2000). Eight hrc genes share high similarity with flagellar genes, suggesting that the T3 apparatus is related to a flagellum (He, 1998). P. syringase HrpA is the major structural protein of the hrp pili, which is much longer than the counterparts in mammalian pathogens, suggesting that hrp pili span thick plant cell wall (Jin et al., 2001; Kubori et al., 1998).

 

Effectors are the T3SS-injected virulence proteins that are responsible for the bacterial pathogenicity. Although no conserved motif can be found in the N-terminal region of multiple effectors, it is believed that the amphipathic nature and the N-terminal amino acid composition of effectors are the secretion signals (Galan and Wolf-Watz, 2006; Arnold et al. 2009; Samudrala et al. 2009). Most effectors of P. syringae reside in the hrp island, where the hrp/hrc genes are flanked by a conserved effector locus (CEL) and an exchangeable effector locus (EEL). The CEL has been shown to be crucial for the bacterial pathogenicity while the EEL only has a minor role (Alfano et al. 2000; Collmer et al. 2000). A handful of effectors are named Avr proteins because they were initially characterized as the proteins that induced the avirulent r本论文由英语论文网提供整理，提供论文代写，英语论文代写，代写论文，代写英语论文，代写留学生论文，代写英文论文，留学生论文代写相关核心关键词搜索。