scholarly journals Erratum: Corrigendum: The Type II Secreted Lipase/Esterase LesA is a Key Virulence Factor Required for Xylella fastidiosa Pathogenesis in Grapevines

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Rafael Nascimento ◽  
Hossein Gouran ◽  
Sandeep Chakraborty ◽  
Hyrum W. Gillespie ◽  
Hebréia O. Almeida-Souza ◽  
...  
Keyword(s):  
Virulence Factor ◽  
Xylella Fastidiosa ◽  
Type Ii ◽  
Secreted Lipase

scholarly journals Xylella fastidiosa Requires Polygalacturonase for Colonization and Pathogenicity in Vitis vinifera Grapevines

2007 ◽  
Vol 20 (4) ◽  
pp. 411-419 ◽  
Author(s):  
M. Caroline Roper ◽  
L. Carl Greve ◽  
Jeremy G. Warren ◽  
John M. Labavitch ◽  
Bruce C. Kirkpatrick
Keyword(s):  
Cell Wall ◽  
Vitis Vinifera ◽  
Virulence Factor ◽  
Plant Cell Wall ◽  
Xylella Fastidiosa ◽  
Cell Wall Degradation ◽  
Cell Wall Degrading Enzymes ◽  
Xylem Elements ◽  
Plant Cell Wall Degradation ◽  
Significant Disease

Xylella fastidiosa is the causal agent of Pierce's disease of grape, an economically significant disease for the grape industry. X. fastidiosa systemically colonizes the xylem elements of grapevines and is able to breach the pit pore membranes separating xylem vessels by unknown mechanisms. We hypothesized that X. fastidiosa utilizes cell wall degrading enzymes to break down pit membranes, based on the presence of genes involved in plant cell wall degradation in the X. fastidiosa genome. These genes include several β-1,4 endoglucanases, several xylanases, several xylosidases, and one polygalacturonase (PG). In this study, we demonstrated that the pglA gene encodes a functional PG. A mutant in pglA lost pathogenicity and was compromised in its ability to systemically colonize Vitis vinifera grapevines. The results indicate that PG is required for X. fastidiosa to successfully infect grapevines and is a critical virulence factor for X. fastidiosa pathogenesis in grapevine.

scholarly journals The Type II Secreted Lipase/Esterase LesA is a Key Virulence Factor Required for Xylella fastidiosa Pathogenesis in Grapevines

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Rafael Nascimento ◽  
Hossein Gouran ◽  
Sandeep Chakraborty ◽  
Hyrum W. Gillespie ◽  
Hebréia O. Almeida-Souza ◽  
...  
Keyword(s):  
Culture Supernatant ◽  
Bacterial Culture ◽  
Xylella Fastidiosa ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Type Ii ◽  
Symptom Development ◽  
Bacterial Titer ◽  
Bacterial Culture Supernatant ◽  
Xylem Elements

Abstract Pierce’s disease (PD) of grapevines is caused by Xylella fastidiosa (Xf), a xylem-limited gamma-proteobacterium that is responsible for several economically important crop diseases. The occlusion of xylem elements and interference with water transport by Xf and its associated biofilm have been posited as the main cause of PD symptom development; however, Xf virulence mechanisms have not been described. Analysis of the Xf secretome revealed a putative lipase/esterase (LesA) that was abundantly secreted in bacterial culture supernatant and was characterized as a protein ortholog of the cell wall-degrading enzyme LipA of Xanthomonas strains. LesA was secreted by Xf and associated with a biofilm filamentous network. Additional proteomic analysis revealed its abundant presence in outer membrane vesicles (OMVs). Accumulation of LesA in leaf regions associated positively with PD symptoms and inversely with bacterial titer. The lipase/esterase also elicited a hypersensitive response in grapevine. Xf lesA mutants were significantly deficient for virulence when mechanically inoculated into grapevines. We propose that Xf pathogenesis is caused by LesA secretion mediated by OMV cargos and that its release and accumulation in leaf margins leads to early stages of observed PD symptoms.

scholarly journals Species-Specific Type II Restriction-Modification System of Xylella fastidiosa Temecula1

2010 ◽  
Vol 76 (12) ◽  
pp. 4092-4095 ◽  
Author(s):  
Ayumi Matsumoto ◽  
Michele M. Igo
Keyword(s):  
Escherichia Coli ◽  
Transformation Efficiency ◽  
Xylella Fastidiosa ◽  
Type Ii ◽  
Modification System ◽  
Restriction Modification System ◽  
Species Specific ◽  
Restriction Modification

ABSTRACT The transformation efficiency of Xylella fastidiosa can be increased by interfering with restriction by the strain-specific type II system encoded by the PD1607 and PD1608 genes. Here, we report results for two strategies: in vitro methylation using M.SssI and isolation of DNA from an Escherichia coli strain expressing the methylase PD1607.

scholarly journals A secreted lipase of Fusarium graminearum is a virulence factor required for infection of cereals

2005 ◽  
Vol 42 (3) ◽  
pp. 364-375 ◽  
Author(s):  
Christian A. Voigt ◽  
Wilhelm Schäfer ◽  
Siegfried Salomon
Keyword(s):  
Fusarium Graminearum ◽  
Virulence Factor ◽  
Secreted Lipase

scholarly journals A Rhamnose-Rich O-Antigen Mediates Adhesion, Virulence, and Host Colonization for the Xylem-Limited Phytopathogen Xylella fastidiosa

2013 ◽  
Vol 26 (6) ◽  
pp. 676-685 ◽  
Author(s):  
Jennifer C. Clifford ◽  
Jeannette N. Rapicavoli ◽  
M. Caroline Roper
Keyword(s):  
Cell Surface ◽  
Virulence Factor ◽  
Xylella Fastidiosa ◽  
Cell Aggregation ◽  
Pierce's Disease ◽  
Core Oligosaccharide ◽  
Gram Negative ◽  
Pierce’S Disease ◽  
O Antigen ◽  
Successful Infection

Xylella fastidiosa is a gram-negative, xylem-limited bacterium that causes a lethal disease of grapevine called Pierce's disease. Lipopolysaccharide (LPS) composes approximately 75% of the outer membrane of gram-negative bacteria and, because it is largely displayed on the cell surface, it mediates interactions between the bacterial cell and its surrounding environment. LPS is composed of a conserved lipid A-core oligosaccharide component and a variable O-antigen portion. By targeting a key O-antigen biosynthetic gene, we demonstrate the contribution of the rhamnose-rich O-antigen to surface attachment, cell–cell aggregation, and biofilm maturation: critical steps for successful infection of the host xylem tissue. Moreover, we have demonstrated that a fully formed O-antigen moiety is an important virulence factor for Pierce's disease development in grape and that depletion of the O-antigen compromises its ability to colonize the host. It has long been speculated that cell-surface polysaccharides play a role in X. fastidiosa virulence and this study confirms that LPS is a major virulence factor for this important agricultural pathogen.

scholarly journals Molecular and phenotypic characteristics of methicillin-resistant Staphylococcus aureus isolated from hospitalized patients

2015 ◽  
Vol 9 (07) ◽  
pp. 743-751 ◽  
Author(s):  
Caio Ferreira de Oliveira ◽  
Alexandre Tadachi Morey ◽  
Jussevania Pereira Santos ◽  
Ludmila Vilela Pereira Gomes ◽  
Juscélio Donizete Cardoso ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factor ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Genetic Relatedness ◽  
Sccmec Type ◽  
Hospitalized Patients ◽  
Type I ◽  
Type Ii ◽  
Methicillin Resistant ◽  
Encoding Genes

Introduction: Methicillin-resistant Staphylococcus aureus (MRSA) is one of the leading causes of infections acquired in both community and hospital settings. In this study, MRSA isolated from different sources of hospitalized patients was characterized by molecular and phenotypic methods. Methodology: A total of 123 S. aureus isolates were characterized according to their genetic relatedness by repetitive element sequence based-PCR (REP-PCR), in vitro antimicrobial susceptibility profile, SCCmec typing and presence of seven virulence factor-encoding genes. Results: REP-PCR fingerprinting showed low relatedness between the isolates, and the predominance of one specific lineage or clonal group was not observed. All isolates were susceptible to teicoplanin and linezolide. All isolates were resistant to cefoxitin and penicillin, and the majority were also resistant to one or more other antimicrobials. Fifty isolates (41.7%) were intermediately resistant to vancomycin. Most isolates harbored SCCmec type II (53.7%), followed by type I (22.8%), type IV (8.1%) and type III (1.6%). All isolates harbored at least two virulence factor-encoding genes, and the prevalence was as follows: coa, 100%; icaA, 100%; hla, 13.0%; hlb, 91.1%, hld, 91.1%; lukS-PV and lukF-PV, 2.4%; and tst, 34.1%. A positive association with the presence of hla and SCCmec type II, and tst and SCCmec type I was observed. Conclusion: This study showed the high virulence potential of multidrug-resistant MRSA circulating in a teaching hospital. A high prevalence of MRSA showing intermediate vancomycin resistance was also observed, indicating the urgent need to improve strategies for controlling the use of antimicrobials for appropriate management of S. aureus infections.

Type II Solar Radio Bursts over Solar Cycle 21

1994 ◽  
Vol 144 ◽  
pp. 283-284
Author(s):  
G. Maris ◽  
E. Tifrea
Keyword(s):  
Solar Radio ◽  
Interplanetary Space ◽  
Impulsive Phase ◽  
Radio Bursts ◽  
Type Ii ◽  
Solar Radio Bursts ◽  
Strong Energy ◽  
Mass Ejection ◽  
Geophysical Effect ◽  
Radio Event

The type II solar radio bursts produced by a shock wave passing through the solar corona are one of the most frequently studied solar activity phenomena. The scientific interest in this type of phenomenon is due to the fact that the presence of this radio event in a solar flare is an almost certain indicator of a future geophysical effect. The origin of the shock waves which produce these bursts is not at all simple; besides the shocks which are generated as a result of a strong energy release during the impulsive phase of a flare, there are also the shocks generated by a coronal mass ejection or the shocks which appear in the interplanetary space due to the supplementary acceleration of the solar particles.

Heat-Etching with a Bullivant Type II Simple Freeze-Cleave Device

1970 ◽  
Vol 28 ◽  
pp. 106-107 ◽  
Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt
Keyword(s):  
New Zealand ◽  
General Hospital ◽  
Massachusetts General Hospital ◽  
Type I ◽  
Type Ii ◽  
Collaborative Effort ◽  
Temperature And Pressure ◽  
The University

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

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