Plant Cell Contact-Dependent Virulence Regulation of hrp Genes in Pseudomonas syringae pv. tabaci 11528

2011 ◽  
Vol 21 (2) ◽  
pp. 227-234 ◽  
Author(s):  
Jun-Seung Lee ◽  
Ji-Young Cha ◽  
Hyung-Suk Baik
Keyword(s):  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Cell Contact ◽  
Virulence Regulation ◽  
Hrp Genes

scholarly journals A Signal Transfer System Through Three Compartments Transduces the Plant Cell Contact-Dependent Signal Controlling Ralstonia solanacearum hrp Genes

2002 ◽  
Vol 15 (2) ◽  
pp. 109-119 ◽  
Author(s):  
Belen Brito ◽  
Didier Aldon ◽  
Patrick Barberis ◽  
Christian Boucher ◽  
Stéphane Genin
Keyword(s):  
Plant Cell ◽  
Ralstonia Solanacearum ◽  
Host Plants ◽  
Plant Cell Wall ◽  
Cell Contact ◽  
Physical Interaction ◽  
Signal Transfer ◽  
Regulatory Cascade ◽  
Hrp Genes ◽  
Dependent Signal

Ralstonia solanacearum hrp genes encode a type III secretion system required for disease development in host plants and for hypersensitive response elicitation on non-hosts. hrp genes are expressed in the presence of plant cells through the HrpB regulator. This activation, which requires physical interaction between the bacteria and the plant cell, is sensed by the outer membrane receptor PrhA. PrhA transduces the plant cell contact-dependent signal through a complex regulatory cascade integrated by the PrhJ, HrpG, and HrpB regulators. In this study, we have identified two genes, named prhI and prhR, that belong to the hrp gene cluster and whose predicted products show homology with extracytoplasmic function sigma factors and transmembrane proteins, respectively. Strains carrying a mutation in prhIR show a delayed pathogenic phenotype toward host plants. PrhIR control the plant cell contact-dependent activation of hrp genes. prhIR gene expression is induced by a signal present in the plant cell co-culture that is not PrhA-dependent. Genetic evidence shows that PrhIR act upstream of PrhJ in the regulatory cascade, likely transducing the signal sensed by PrhA through the periplasm as described for signal transfer systems through three compartments. This is the first report of such a surface signaling mechanism activating pathogenicity determinants in response to a nondiffusible plant cell wall signal.

scholarly journals BAK1 Is Not a Target of the Pseudomonas syringae Effector AvrPto

2011 ◽  
Vol 24 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Tingting Xiang ◽  
Na Zong ◽  
Jie Zhang ◽  
Jinfeng Chen ◽  
Mingsheng Chen ◽  
...  
Keyword(s):  
Cell Surface ◽  
Immune Responses ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Crucial Role ◽  
Pathogenic Bacteria ◽  
Effector Proteins ◽  
Receptor Like Kinase ◽  
Receptor Kinases ◽  
New Evidence

Plant cell surface-localized receptor kinases such as FLS2, EFR, and CERK1 play a crucial role in detecting invading pathogenic bacteria. Upon stimulation by bacterium-derived ligands, FLS2 and EFR interact with BAK1, a receptor-like kinase, to activate immune responses. A number of Pseudomonas syringae effector proteins are known to block immune responses mediated by these receptors. Previous reports suggested that both FLS2 and BAK1 could be targeted by the P. syringae effector AvrPto to inhibit plant defenses. Here, we provide new evidence further supporting that FLS2 but not BAK1 is targeted by AvrPto in plants. The AvrPto-FLS2 interaction prevented the phosphorylation of BIK1, a downstream component of the FLS2 pathway.

Organization, regulation and function of Pseudomonas syringae pv. syringae hrp genes

1994 ◽  
pp. 593-603 ◽  
Author(s):  
Steven W. Hutcheson ◽  
Sunggi Heu ◽  
Hsiou-Chen Huang ◽  
Michael C. Lidell ◽  
Yingxian Xiao
Keyword(s):  
Pseudomonas Syringae ◽  
Hrp Genes ◽  
And Function

scholarly journals Plasmodesmata-Related Structural and Functional Proteins: The Long Sought-After Secrets of a Cytoplasmic Channel in Plant Cell Walls

2019 ◽  
Vol 20 (12) ◽  
pp. 2946 ◽  
Author(s):  
Xiao Han ◽  
Li-Jun Huang ◽  
Dan Feng ◽  
Wenhan Jiang ◽  
Wenzhuo Miu ◽  
...  
Keyword(s):  
Cell Wall ◽  
Plant Cell ◽  
Cell Walls ◽  
Plasma Membranes ◽  
Plant Cell Wall ◽  
Plant Cells ◽  
Protein Composition ◽  
Cell Contact ◽  
Plant Cell Walls ◽  
Cell Organelles

Plant cells are separated by cellulose cell walls that impede direct cell-to-cell contact. In order to facilitate intercellular communication, plant cells develop unique cell-wall-spanning structures termed plasmodesmata (PD). PD are membranous channels that link the cytoplasm, plasma membranes, and endoplasmic reticulum of adjacent cells to provide cytoplasmic and membrane continuity for molecular trafficking. PD play important roles for the development and physiology of all plants. The structure and function of PD in the plant cell walls are highly dynamic and tightly regulated. Despite their importance, plasmodesmata are among the few plant cell organelles that remain poorly understood. The molecular properties of PD seem largely elusive or speculative. In this review, we firstly describe the general PD structure and its protein composition. We then discuss the recent progress in identification and characterization of PD-associated plant cell-wall proteins that regulate PD function, with particular emphasis on callose metabolizing and binding proteins, and protein kinases targeted to and around PD.

scholarly journals Pectobacterium carotovorum Elicits Plant Cell Death with DspE/F but the P. carotovorum DspE Does Not Suppress Callose or Induce Expression of Plant Genes Early in Plant–Microbe Interactions

2011 ◽  
Vol 24 (7) ◽  
pp. 773-786 ◽  
Author(s):  
Hye-Sook Kim ◽  
Phanit Thammarat ◽  
Steven A. Lommel ◽  
Clifford S. Hogan ◽  
Amy O. Charkowski
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Secretion System ◽  
Broad Host Range ◽  
Pectobacterium Carotovorum ◽  
Callose Deposition

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.

scholarly journals Immunogold Labeling of Hrp Pili of Pseudomonas syringae pv. tomato Assembled in Minimal Medium and In Planta

2001 ◽  
Vol 14 (2) ◽  
pp. 234-241 ◽  
Author(s):  
Wenqi Hu ◽  
Jing Yuan ◽  
Qiao-Ling Jin ◽  
Patrick Hart ◽  
Sheng Yang He
Keyword(s):  
Arabidopsis Thaliana ◽  
Pseudomonas Syringae ◽  
Minimal Medium ◽  
Leaf Tissue ◽  
Hypersensitive Reaction ◽  
Immunogold Labeling ◽  
Structural Protein ◽  
In Planta ◽  
Hrp Genes

Hypersensitive reaction and pathogenicity (hrp) genes are required for Pseudomonas syringae pv. tomato (Pst) DC3000 to cause disease in susceptible tomato and Arabidopsis thaliana plants and to elicit the hypersensitive response in resistant plants. The hrp genes encode a type III protein secretion system known as the Hrp system, which in Pst DC3000 secretes HrpA, HrpZ, HrpW, and AvrPto and assembles a surface appendage, named the Hrp pilus, in hrp-gene-inducing minimal medium. HrpA has been suggested to be the Hrp pilus structural protein on the basis of copurification and mutational analyses. In this study, we show that an antibody against HrpA efficiently labeled Hrp pili, whereas antibodies against HrpW and HrpZ did not. Immunogold labeling of bacteria-infected Arabidopsis thaliana leaf tissue with an Hrp pilus antibody revealed a characteristic lineup of gold particles around bacteria and/or at the bacterium-plant contact site. These results confirm that HrpA is the major structural protein of the Hrp pilus and provide evidence that Hrp pili are assembled in vitro and in planta.

scholarly journals Immunocytochemical Localization of HrpA and HrpZ Supports a Role for the Hrp Pilus in the Transfer of Effector Proteins from Pseudomonas syringae pv. tomato Across the Host Plant Cell Wall

2001 ◽  
Vol 14 (3) ◽  
pp. 394-404 ◽  
Author(s):  
Ian R. Brown ◽  
John W. Mansfield ◽  
Suvi Taira ◽  
Elina Roine ◽  
Martin Romantschuk
Keyword(s):  
Cell Wall ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Type Iii Secretion ◽  
Plant Cell Wall ◽  
Immunogold Labeling ◽  
Effector Proteins ◽  
Basal Bodies ◽  
Type Iii

The Hrp pilus, composed of HrpA subunits, is an essential component of the type III secretion system in Pseudomonas syringae. We used electron microscopy (EM) and immunocytochemistry to examine production of the pilus in vitro from P. syringae pv. tomato strain DC3000 grown under hrp-inducing conditions on EM grids. Pili, when labeled with antibodies to HrpA, developed rapidly in a nonpolar manner shortly after the detection of the hrpA transcript and extended up to 5 μm into surrounding media. Structures at the base of the pilus were clearly differentiated from the basal bodies of flagella. The HrpZ protein, also secreted via the type III system, was found by immunogold labeling to be associated with the pilus in vitro. Accumulation and secretion of HrpA and HrpZ were also examined quantitatively after the inoculation of wild-type DC3000 and hrpA and hrpZ mutants into leaves of Arabidopsis thaliana. The functional pilus crossed the plant cell wall to generate tracks of immunogold labeling for HrpA and HrpZ. Mutants that produced HrpA but did not assemble pili were nonpathogenic, did not secrete HrpA protein, and were compromised for the accumulation of HrpZ. A model is proposed in which the rapidly elongating Hrp pilus acts as a moving conveyor, facilitating transfer of effector proteins from bacteria to the plant cytoplasm across the formidable barrier of the plant cell wall.

scholarly journals Bacterial Growth Restriction During Host Resistance to Pseudomonas syringae Is Associated with Leaf Water Loss and Localized Cessation of Vascular Activity in Arabidopsis thaliana

2009 ◽  
Vol 22 (7) ◽  
pp. 857-867 ◽  
Author(s):  
Brian C. Freeman ◽  
Gwyn A. Beattie
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Bacterial Growth ◽  
Water Loss ◽  
Leaf Water ◽  
Infection Site ◽  
Vascular Activity ◽  
Leaf Water Loss

The physiological mechanisms by which plants limit the growth of bacterial pathogens during gene-for-gene resistance are poorly understood. We characterized early events in the Arabidopsis thaliana–Pseudomonas syringae pathosystem to identify physiological changes for which the kinetics are consistent with bacterial growth restriction. Using a safranine-O dye solution to detect vascular activity, we demonstrated that A. thaliana Col-0 resistance to P. syringae pv. tomato DC3000 cells expressing avrRpm1 involved virtually complete cessation of vascular water movement into the infection site within only 3 h postinoculation (hpi), under the conditions tested. This vascular restriction preceded or was simultaneous with precipitous decreases in photosynthesis, stomatal conductance, and leaf transpiration, with the latter two remaining at detectable levels. Microscopic plant cell death was detected as early as 2 hpi. Interestingly, suppression of bacterial growth during AvrRpm1-mediated resistance was eliminated by physically blocking leaf water loss through the stomata without altering plant cell death and was nearly eliminated by incubating plants at high relative humidity. The majority of the population growth benefit from blocking leaf water loss occurred early after inoculation, i.e., between 4 and 8 hpi. Collectively, these results support a model in which A. thaliana suppresses P. syringae growth during gene-for-gene resistance, at least in part, by coupling restricted vascular flow to the infection site with water loss through partially open stomata; that is, the plants effectively starve the invading bacteria for water.

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