Exploring the expression and functionality of the rsm sRNAs in Pseudomonas syringae pv. tomato DC3000

Diverse gene products including phytotoxins, pathogen-associated molecular patterns, and type III secreted effectors influence interactions between Pseudomonas syringae strains and plants, with additional yet uncharacterized factors likely contributing as well. Of particular interest are those interactions governing pathogen-host specificity. Comparative genomics of closely related pathogens with different host specificity represents an excellent approach for identification of genes contributing to host-range determination. A draft genome sequence of Pseudomonas syringae pv. tomato T1, which is pathogenic on tomato but nonpathogenic on Arabidopsis thaliana, was obtained for this purpose and compared with the genome of the closely related A. thaliana and tomato model pathogen P. syringae pv. tomato DC3000. Although the overall genetic content of each of the two genomes appears to be highly similar, the repertoire of effectors was found to diverge significantly. Several P. syringae pv. tomato T1 effectors absent from strain DC3000 were confirmed to be translocated into plants, with the well-studied effector AvrRpt2 representing a likely candidate for host-range determination. However, the presence of avrRpt2 was not found sufficient to explain A. thaliana resistance to P. syringae pv. tomato T1, suggesting that other effectors and possibly type III secretion system–independent factors also play a role in this interaction.

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Expression of a RING-HC protein from rice improves resistance to Pseudomonas syringae pv. tomato DC3000 in transgenic Arabidopsis thaliana

Journal of Experimental Botany ◽

10.1093/jxb/erm272 ◽

2007 ◽

Vol 58 (15-16) ◽

pp. 4147-4159 ◽

Cited By ~ 27

Author(s):

M.-Y. Cheung ◽

N.-Y. Zeng ◽

S.-W. Tong ◽

F. Wing-Yen Li ◽

K.-J. Zhao ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Pseudomonas Syringae ◽

Transgenic Arabidopsis ◽

Tomato Dc3000 ◽

Transgenic Arabidopsis Thaliana

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Chitosan Oligosaccharide Induces Resistance to Pseudomonas syringae pv. tomato DC3000 in Arabidopsis thaliana by Activating Both Salicylic Acid– and Jasmonic Acid–Mediated Pathways

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-03-18-0071-r ◽

2018 ◽

Vol 31 (12) ◽

pp. 1271-1279 ◽

Cited By ~ 21

Author(s):

Xiaochen Jia ◽

Haihong Zeng ◽

Wenxia Wang ◽

Fuyun Zhang ◽

Heng Yin

Keyword(s):

Salicylic Acid ◽

Jasmonic Acid ◽

Induced Resistance ◽

Pseudomonas Syringae ◽

Plant Immunity ◽

Chitosan Oligosaccharide ◽

Induction Effect ◽

Tomato Dc3000 ◽

Expression Of Genes ◽

Underlying Mechanisms

Chitosan oligosaccharide (COS) is an effective plant immunity elicitor; however, its induction mechanism in plants is complex and needs further investigation. In this study, the Arabidopsis–Pseudomonas syringae pv. tomato DC3000 (hereafter called DC3000) interaction was used to investigate the induction effect and the underlying mechanisms of COS. COS is effective in inducing resistance to DC3000 in Arabidopsis, and our results demonstrate that treatment with COS 3 days before DC3000 inoculation provided the most effective resistance. Disease severity in jar1 (jasmonic acid [JA]-deficient mutant), NahG, and sid2 (salicylic acid [SA]-deficient mutants) suggest both the SA and JA pathways are required for the Arabidopsis response to DC3000. COS pretreatment induced resistance in wild type (WT), jar1, and also, although to a lesser degree, in NahG and sid2 plants, implying that the SA and JA pathways play redundant roles in COS-induced resistance to DC3000. In COS-pretreated plants, expression of genes related to the SA pathway (PR1, PR2, and PR5) and SA content increased in both WT and jar1. Moreover, expression of genes related to the JA pathway (PDF1.2 and VSP2) and JA content both increased in WT and NahG. In conclusion, COS induces resistance to DC3000 in Arabidopsis by activating both SA- and JA-mediated pathways, although SA and JA pathways play redundant roles in this COS-induced resistance.

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Tomato Stress-Associated Protein 4 Contributes Positively to Immunity Against Necrotrophic Fungus Botrytis cinerea

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-04-18-0097-r ◽

2019 ◽

Vol 32 (5) ◽

pp. 566-582 ◽

Cited By ~ 3

Author(s):

Shixia Liu ◽

Xi Yuan ◽

Yuyan Wang ◽

Hui Wang ◽

Jiali Wang ◽

...

Keyword(s):

Botrytis Cinerea ◽

Pseudomonas Syringae ◽

Expression Patterns ◽

Plant Stress ◽

Oxygen Species ◽

Virus Induced Gene Silencing ◽

Tomato Dc3000 ◽

Enhanced Resistance ◽

Stress Associated Protein ◽

Associated Proteins

Stress-associated proteins (SAPs) are A20 and AN1 domain–containing proteins, some of which play important roles in plant stress signaling. Here, we report the involvement of tomato SlSAP family in immunity. SlSAPs responded with different expression patterns to Botrytis cinerea and defense signaling hormones. Virus-induced gene silencing of each of the SlSAP genes and disease assays revealed that SlSAP4 and SlSAP10 play roles in immunity against B. cinerea. Silencing of SlSAP4 resulted in attenuated immunity to B. cinerea, accompanying increased accumulation of reactive oxygen species and downregulated expression of jasmonate and ethylene (JA/ET) signaling-responsive defense genes. Transient expression of SlSAP4 in Nicotiana benthamiana led to enhanced resistance to B. cinerea. Exogenous application of methyl jasmonate partially restored the resistance of the SlSAP4-silenced plants against B. cinerea. SlSAP4 interacted with three of four SlRAD23 proteins. The A20 domain in SlSAP4 and the Ub-associated domains in SlRAD23d are critical for SlSAP4-SlRAD23d interaction. Silencing of SlRAD23d led to decreased resistance to B. cinerea, but silencing of each of other SlRAD23s did not affect immunity against B. cinerea. Furthermore, silencing of SlSAP4 and each of the SlRAD23s did not affect immunity to Pseudomonas syringae pv. tomato DC3000. These data suggest that SlSAP4 contributes positively to tomato immunity against B. cinereal through affecting JA/ET signaling and may be involved in the substrate ubiquitination process via interacting with SlRAD23d.

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