Pectobacterium carotovorumElicits Plant Cell Death with DspE/F but theP. carotovorumDspE Does Not Suppress Callose or Induce Expression of Plant Genes Early in Plant–Microbe Interactions

Abstract

The broad-host-range bacterial soft rot pathogen Pectobacterium carotovorum causes a DspE/F-dependent plant cell death on Nicotiana benthamiana within 24 h postinoculation (hpi) followed by leaf maceration within 48 hpi. P. carotovorum strains with mutations in type III secretion system (T3SS) regulatory and structural genes, including the dspE/F operon, did not cause hypersensitive response (HR)-like cell death and or leaf maceration. A strain with a mutation in the type II secretion system caused HR-like plant cell death but no maceration. P. carotovorum was unable to impede callose deposition in N. benthamiana leaves, suggesting that P. carotovorum does not suppress this basal immunity function. Within 24 hpi, there was callose deposition along leaf veins and examination showed that the pathogen cells were localized along the veins. To further examine HR-like plant cell death induced by P. carotovorum, gene expression profiles in N. benthamiana leaves inoculated with wild-type and mutant P. carotovorum and Pseudomonas syringae strains were compared. The N. benthamiana gene expression profile of leaves infiltrated with Pectobacterium carotovorum was similar to leaves infiltrated with a Pseudomonas syringae T3SS mutant. These data support a model where Pectobacterium carotovorum uses the T3SS to induce plant cell death in order to promote leaf maceration rather than to suppress plant immunity.

The Role of Secretion Systems and Small Molecules in Soft-Rot Enterobacteriaceae Pathogenicity

“…An exception to this occurs when Pectobacterium is infiltrated into the leaves of solanaceous plants, where it causes a cell death response that is dependent upon DspE. This plant cell death can progress to disease, suggesting that elicitation of programmed cell death in plant leaves promotes virulence of this necrotrophic pathogen (77). Similar phenomena have been seen with other necrotrophs (48,146,152).…”

“…Unlike P. syringae which can have up to 30 potential type III--secreted effector proteins in individual strains, SRE appear to have relatively few (77), including a small number of harpins or helper proteins and the single known effector, DspA/E. The DspE allele in SRE is smaller than homologs found in other phytopathogenic bacteria, such as Erwinia amylovora, and unlike other DspE alleles, it is unable to inhibit callose formation in leaves (77). Deletion of the T3SS from Pectobacterium or Dickeya has only subtle effects on virulence in some pathosystems (58,157).…”

Understanding Plant Immunity as a Surveillance System to Detect Invasion

“…Attempts to separate Victoria blight susceptibility from crown rust resistance have been unsuccessful, suggesting that Pc2 and Vb are the same immune receptor gene (95). Additional examples of necrotrophic effectors used to incite cell death and promote disease have been reported (39,78). The molecular components and pathways determining plant-necrotroph or plant-biotroph interactions are generally the same, but how the responses affect the outcomes of the interactions are in stark contrast.…”

Phytophthora infestans RXLR effector AVR1 interacts with exocyst component Sec5 to manipulate plant immunity

“…Lesion areas were determined at 6 dai. Pst DhrcC was grown at 28°C in King's B medium and resuspended to optical density at 600 nm of 0.5 (approximately 1 3 10 8 colony-forming units mL 21 ) in 10 mM MgCl 2 before infiltration into N. benthamiana leaves (Kim et al, 2011).…”