Role of the Hrp type III protein secretion system in growth of Pseudomonas syringae pv. syringae B728a on host plants in the field

Abstract

ABSTRACThrp genes are reportedly required for pathogenicity in Pseudomonas syringae pv. syringae (Pss) and other phytopathogenic bacterial species. A subset of these genes encodes a type III secretion system through which virulence factors are thought to be delivered to plant cells. In this study, we sought to better understand the role that hrp genes play in interactions of Pss with its host as they occur naturally under field conditions. Population sizes of hrp mutants with defects in genes that encode components of the Hrp secretion system (⌬hrcC::nptII and hrpJ:: ⍀Spc) and a protein secreted via the system (⌬hrpZ::nptII) were similar to B728a on germinating seeds. However, phyllosphere (i.e., leaf) population sizes of the hrcC and hrpJ secretion mutants, but not the hrpZ mutant, were significantly reduced relative to B728a. Thus, the Hrp type III secretion system, but not HrpZ, plays an important role in enabling Pss to f lourish in the phyllosphere, but not the spermosphere. The hrcC and hrpJ mutants caused brown spot lesions on primary leaves at a low frequency when they were inoculated onto seeds at the time of planting. Pathogenic reactions also were found when the hrp secretion mutants were co-infiltrated into bean leaves with a non-lesion-forming gacS mutant of B728a. In both cases, the occurrence of disease was associated with elevated population sizes of the hrp secretion mutants. The role of the Hrp type III secretion system in pathogenicity appears to be largely mediated by its requirement for growth of Pss in the phyllosphere. Without growth, disease does not occur.

The social evolution of bacterial pathogenesis

“…This can be tested with simple co-infection experiments. Such cheating has been experimentally observed among toxins (Waalwijk et al 1983), siderophores (Wolf & Crosa 1986), type III secretion systems (Hirano et al 1999) and even some pili (Hammar et al 1996;Wall et al 1998). Second, the hypothesis predicts that there is a signi¢cant metabolic cost to virulence-factor production.…”

“…Such a cost can be measured in vivo by the ability of cheaters to increase in frequency when rare (e.g. Hirano et al 1999) or in vitro with competition experiments under laboratory conditions that induce production of the virulence factor. Finally, the hypothesis predicts that cheaters reduce the ¢tness of producing strains when the virulence factor is non-transmissible and that horizontal transfer reduces the ¢tness burden of cheaters.…”

Regulation of Bacterial Virulence by Csr (Rsm) Systems

“…As is the case for many other plant and animal pathogens, P. syringae secretes a variety of products, including quorum-sensing compounds, phytotoxins, antibiotics, exoproteases, fluorescent pigments, and alginate, which influence infection and disease processes (363). These secreted products as well as biofilm formation, host colonization, and lesion formation are all regulated by the GacS/GacA TCS (364)(365)(366)(367)(368)(369)(370)(371)(372)(373)(374)(375)(376)(377)(378)(379). Furthermore, genetic analyses of various P. syringae pathovars have identified homologs of the RsmA-inhibitory sRNAs RsmX, RsmY, and RsmZ of P. fluorescens, as well as RsmB of P. carotovorum (55).…”

Bacteria in the Leaf Ecosystem with Emphasis onPseudomonas syringae—a Pathogen, Ice Nucleus, and Epiphyte

“…To address this question, we fieldtested three hrp mutants of P. syringae pv. syringae strain B728a (⌬hrpZ::nptII, ⌬hrcC::nptII, and hrpJ::⍀Spc) (106) (Fig. 14).…”