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Journal articles on the topic 'Induced systemic resistance'

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Published: 4 June 2021

Last updated: 9 March 2023

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1

Cohen, Y. "Systemic induced resistance." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S122—S125. http://dx.doi.org/10.17221/10334-pps.

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Biotic and abiotic agents may induce resistance in plants against pathogens. Abiotic agents may be synthetic or natural. The natural, non-protein amino acid BABA (DL-β-aminobutyric acid) induces systemic resistance in crop plants against pathogens. Dry, killed mycelia of Penicillium chrysogenum (DM) induces local resistance in plants against soil-borne pathogens. The activity of BABA and DM are described here in detail. Both products were shown to effectively control plant disease in nature.

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2

Vallad, Gary E., and Robert M. Goodman. "Systemic Acquired Resistance and Induced Systemic Resistance in Conventional Agriculture." Crop Science 44, no. 6 (November 2004): 1920–34. http://dx.doi.org/10.2135/cropsci2004.1920.

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3

Pieterse, Corné M. J., Christos Zamioudis, Roeland L. Berendsen, David M. Weller, Saskia C. M. Van Wees, and Peter A. H. M. Bakker. "Induced Systemic Resistance by Beneficial Microbes." Annual Review of Phytopathology 52, no. 1 (August 4, 2014): 347–75. http://dx.doi.org/10.1146/annurev-phyto-082712-102340.

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4

Bonello, Gordon, and Storer. "Systemic induced resistance in Monterey pine." Forest Pathology 31, no. 2 (April 28, 2001): 99–106. http://dx.doi.org/10.1046/j.1439-0329.2001.00230.x.

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5

van Loon, L. C., P. A. H. M. Bakker, and C. M. J. Pieterse. "SYSTEMIC RESISTANCE INDUCED BY RHIZOSPHERE BACTERIA." Annual Review of Phytopathology 36, no. 1 (September 1998): 453–83. http://dx.doi.org/10.1146/annurev.phyto.36.1.453.

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6

Thomashow, Linda S. "Induced systemic resistance: a delicate balance." Environmental Microbiology Reports 8, no. 5 (October 2016): 560–63. http://dx.doi.org/10.1111/1758-2229.12474.

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7

Bakker, Peter A. H. M., Rogier F. Doornbos, Christos Zamioudis, Roeland L. Berendsen, and Corne M. J. Pieterse. "Induced Systemic Resistance and the Rhizosphere Microbiome." Plant Pathology Journal 29, no. 2 (June 1, 2013): 136–43. http://dx.doi.org/10.5423/ppj.si.07.2012.0111.

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8

Schweizer, Patrick, Antony Buchala, Robert Dudler, and Jean-Pierre Métraux. "Induced systemic resistance in wounded rice plants." Plant Journal 14, no. 4 (May 1998): 475–81. http://dx.doi.org/10.1046/j.1365-313x.1998.00141.x.

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9

Simms, Ellen L., and Todd J. Vision. "Pathogen-induced systemic resistance in Ipomoea purpurea." Oecologia 102, no. 4 (1995): 494–500. http://dx.doi.org/10.1007/bf00341362.

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10

Bakker, Peter A. H. M., Corné M. J. Pieterse, and L. C. van Loon. "Induced Systemic Resistance by Fluorescent Pseudomonas spp." Phytopathology® 97, no. 2 (February 2007): 239–43. http://dx.doi.org/10.1094/phyto-97-2-0239.

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Fluorescent Pseudomonas spp. have been studied for decades for their plant growth-promoting effects through effective suppression of soilborne plant diseases. The modes of action that play a role in disease suppression by these bacteria include siderophore-mediated competition for iron, antibiosis, production of lytic enzymes, and induced systemic resistance (ISR). The involvement of ISR is typically studied in systems in which the Pseudomonas bacteria and the pathogen are inoculated and remain spatially separated on the plant, e.g., the bacteria on the root and the pathogen on the leaf, or by use of split root systems. Since no direct interactions are possible between the two populations, suppression of disease development has to be plant-mediated. In this review, bacterial traits involved in Pseudomonas-mediated ISR will be discussed.

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11

De Meyer, Geert, Kristof Capieau, Kris Audenaert, Antony Buchala, Jean-Pierre Métraux, and Monica Höfte. "Nanogram Amounts of Salicylic Acid Produced by the Rhizobacterium Pseudomonas aeruginosa 7NSK2 Activate the Systemic Acquired Resistance Pathway in Bean." Molecular Plant-Microbe Interactions® 12, no. 5 (May 1999): 450–58. http://dx.doi.org/10.1094/mpmi.1999.12.5.450.

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Root colonization by specific nonpathogenic bacteria can induce a systemic resistance in plants to pathogen infections. In bean, this kind of systemic resistance can be induced by the rhizobacterium Pseudomonas aeruginosa 7NSK2 and depends on the production of salicylic acid by this strain. In a model with plants grown in perlite we demonstrated that Pseudomonas aeruginosa 7NSK2-induced resistance is equivalent to the inclusion of 1 nM salicylic acid in the nutrient solution and used the latter treatment to analyze the molecular basis of this phenomenon. Hydroponic feeding of 1 nM salicylic acid solutions induced phenylalanine ammonia-lyase activity in roots and increased free salicylic acid levels in leaves. Because pathogen-induced systemic acquired resistance involves similar changes it was concluded that 7NSK2-induced resistance is mediated by the systemic acquired resistance pathway. This conclusion was validated by analysis of phenylalanine ammonia-lyase activity in roots and of salicylic acid levels in leaves of soil-grown plants treated with Pseudomonas aeruginosa. The induction of systemic acquired resistance by nanogram amounts of salicylic acid is discussed with respect to long-distance signaling in systemic acquired resistance.

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12

Acharya, R., P. Patra, N. Chakraborty, N. S. Gupta, and K. Acharya. "Footprint of Nitric oxide in induced systemic resistance." NBU Journal of Plant Sciences 7, no. 1 (2013): 55–61. http://dx.doi.org/10.55734/nbujps.2013.v07i01.008.

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Nitric oxide (NO) is a potent signaling molecule with diverse physiological functions in plants. Several rhizobacterial strains may have capacity to induce systemic resistance in (ISR) plants but how far the biochemical mechanisms in which No participates in this signaling pathway is still an open question. The present study have shown in Pseudomonas aeruginosa WS-1 mediated ISR inducing system in Catharanthus roseus induces defense enzyme and phenolics and also showed a two fold increase in NO production when challenge with Alternaria alternata. Furthermore, NO donor treatment in the host produced same defense molecules in a comparable manner. From those observations it is suggested that NO might have possible signaling role in ISR during crosstalk between the ISR inducing agent and pathogen within the host system.

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13

Uknes, S., T. Delaney, B. Vernooij, L. Friedrich, S. Williams, D. Chandler, K. Weymann, et al. "1007 SYSTEMIC ACQUIRED RESISTANCE." HortScience 29, no. 5 (May 1994): 573g—574. http://dx.doi.org/10.21273/hortsci.29.5.573g.

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Systemic acquired resistance is a broad spectrum inducible defense response that is associated with the expression of a set of genes (SAR genes). Expression of one of these genes (PR-1a from tobacco) in transgenic tobacco confers increased tolerance to two oomycete pathogens. A direct role for salicylic acid (SA) in signaling SAR has been established in tobacco by analysis of transgenic tobacco expressing salicylate hydroxylase (SAH, an enzyme that inactivates SA by conversion to catechol). Tobacco plants that express SAH are blocked in the accumulation of SA and the development of SAR when responding lo TMV. Furthermore, both Arabidopsis and tobacco expressing SAH have altered pathogen induced lesion morphology, exemplified by larger spreading lesions. Putative mutants in SAR gene expression were isolated by screening M2 Arabidopsis plants for altered expression of PR-1 and PR-2 or for sensitivity to pathogen infection following INA treatment. The putative mutants all into two major classes,constitutive (cim, constitutive immunity) and non-inducible (nim, non-inducible immunity). Several cim mutants exhibits a disease lesion phenotype in the absence of pathogen.

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14

Yan, Zhinong, M. S. Reddy, Choong-Min Ryu, John A. McInroy, Mark Wilson, and Joseph W. Kloepper. "Induced Systemic Protection Against Tomato Late Blight Elicited by Plant Growth-Promoting Rhizobacteria." Phytopathology® 92, no. 12 (December 2002): 1329–33. http://dx.doi.org/10.1094/phyto.2002.92.12.1329.

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Two strains of plant growth-promoting rhizobacteria (PGPR), Bacillus pumilus SE34 and Pseudomonas fluorescens 89B61, elicited systemic protection against late blight on tomato and reduced disease severity by a level equivalent to systemic acquired resistance induced by Phytophthora infestans or induced local resistance by chemical inducer β-amino butyric acid (BABA) in greenhouse assays. Germination of sporangia and zoospores of P. infestans on leaf surfaces of tomato plants treated with the two PGPR strains, pathogen, and chemical BABA was significantly reduced compared with the noninduced control. Induced protection elicited by PGPR, pathogen, and BABA were examined to determine the signal transduction pathways in three tomato lines: salicylic acid (SA)-hydroxylase transgenic tomato (nahG), ethylene insensitive mutants (Nr/Nr), and jasmonic acid insensitive mutants (def1). Results suggest that induced protection elicited by both bacilli and pseudomonad PGPR strains was SA-independent but ethylene- and jasmonic acid-dependent, whereas systemic acquired resistance elicited by the pathogen and induced local resistance by BABA were SA-dependent. The lack of colonization of tomato leaves by strain 89B61 suggests that the observed induced systemic resistance (ISR) was due to systemic protection by strain 89B61 and not attributable to a direct interaction between pathogen and biological control agent. Although strain SE34 was detected on tomato leaves, ISR mainly accounted for the systemic protection with this strain.

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15

Zhao, Pan, Lu Liu, Jingjing Cao, Zhiqin Wang, Yonglong Zhao, and Naiqin Zhong. "Transcriptome Analysis of Tryptophan-Induced Resistance against Potato Common Scab." International Journal of Molecular Sciences 23, no. 15 (July 29, 2022): 8420. http://dx.doi.org/10.3390/ijms23158420.

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Potato common scab (CS) is a worldwide soil-borne disease that severely reduces tuber quality and market value. We observed that foliar application of tryptophan (Trp) could induce resistance against CS. However, the mechanism of Trp as an inducer to trigger host immune responses is still unclear. To facilitate dissecting the molecular mechanisms, the transcriptome of foliar application of Trp and water (control, C) was compared under Streptomyces scabies (S) inoculation and uninoculation. Results showed that 4867 differentially expressed genes (DEGs) were identified under S. scabies uninoculation (C-vs-Trp) and 2069 DEGs were identified under S. scabies inoculation (S-vs-S+Trp). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that Trp induced resistance related to the metabolic process, response to stimulus, and biological regulation. As phytohormone metabolic pathways related to inducing resistance, the expression patterns of candidate genes involved in salicylic acid (SA) and jasmonic acid/ethylene (JA/ET) pathways were analyzed using qRT-PCR. Their expression patterns showed that the systemic acquired resistance (SAR) and induced systemic resistance (ISR) pathways could be co-induced by Trp under S. scabies uninoculation. However, the SAR pathway was induced by Trp under S. scabies inoculation. This study will provide insights into Trp-induced resistance mechanisms of potato for controlling CS, and extend the application methods of Trp as a plant resistance inducer in a way that is cheap, safe, and environmentally friendly.

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16

Zhu, Yun J., Xiaohui Qiu, Paul H. Moore, Wayne Borth, John Hu, Stephen Ferreira, and Henrik H. Albert. "Systemic acquired resistance induced by BTH in papaya." Physiological and Molecular Plant Pathology 63, no. 5 (November 2003): 237–48. http://dx.doi.org/10.1016/j.pmpp.2004.03.003.

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17

Nawrocka, J., and U. Małolepsza. "Diversity in plant systemic resistance induced by Trichoderma." Biological Control 67, no. 2 (November 2013): 149–56. http://dx.doi.org/10.1016/j.biocontrol.2013.07.005.

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18

Pieterse, C. M. J., S. C. M. Van Wees, J. Ton, J. A. Van Pelt, and L. C. Van Loon. "Signalling in Rhizobacteria-Induced Systemic Resistance inArabidopsis thaliana." Plant Biology 4, no. 5 (September 2002): 535–44. http://dx.doi.org/10.1055/s-2002-35441.

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19

Cameron, Robin K., Richard A. Dixon, and Christopher J. Lamb. "Biologically induced systemic acquired resistance in Arabidopsis thaliana." Plant Journal 5, no. 5 (May 1994): 715–25. http://dx.doi.org/10.1111/j.1365-313x.1994.00715.x.

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20

Tonelli, María Laura, María Soledad Figueredo, Johan Rodríguez, Adriana Fabra, and Fernando Ibañez. "Induced systemic resistance -like responses elicited by rhizobia." Plant and Soil 448, no. 1-2 (January 11, 2020): 1–14. http://dx.doi.org/10.1007/s11104-020-04423-5.

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21

Weete, John D. "Induced systemic resistance to Alternaria cassiae in sicklepod." Physiological and Molecular Plant Pathology 40, no. 6 (June 1992): 437–45. http://dx.doi.org/10.1016/0885-5765(92)90034-s.

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22

Lenk, Miriam, Marion Wenig, Kornelia Bauer, Florian Hug, Claudia Knappe, Birgit Lange, Timsy, et al. "Pipecolic Acid Is Induced in Barley upon Infection and Triggers Immune Responses Associated with Elevated Nitric Oxide Accumulation." Molecular Plant-Microbe Interactions® 32, no. 10 (October 2019): 1303–13. http://dx.doi.org/10.1094/mpmi-01-19-0013-r.

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Pipecolic acid (Pip) is an essential component of systemic acquired resistance, priming resistance in Arabidopsis thaliana against (hemi)biotrophic pathogens. Here, we studied the potential role of Pip in bacteria-induced systemic immunity in barley. Exudates of barley leaves infected with the systemic immunity–inducing pathogen Pseudomonas syringae pv. japonica induced immune responses in A. thaliana. The same leaf exudates contained elevated Pip levels compared with those of mock-treated barley leaves. Exogenous application of Pip induced resistance in barley against the hemibiotrophic bacterial pathogen Xanthomonas translucens pv. cerealis. Furthermore, both a systemic immunity–inducing infection and exogenous application of Pip enhanced the resistance of barley against the biotrophic powdery mildew pathogen Blumeria graminis f. sp. hordei. In contrast to a systemic immunity-inducing infection, Pip application did not influence lesion formation by a systemically applied inoculum of the necrotrophic fungus Pyrenophora teres. Nitric oxide (NO) levels in barley leaves increased after Pip application. Furthermore, X. translucens pv. cerealis induced the accumulation of superoxide anion radicals and this response was stronger in Pip-pretreated compared with mock-pretreated plants. Thus, the data suggest that Pip induces barley innate immune responses by triggering NO and priming reactive oxygen species accumulation.

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23

Wu, Gengwei, Yunpeng Liu, Yu Xu, Guishan Zhang, Qirong Shen, and Ruifu Zhang. "Exploring Elicitors of the Beneficial Rhizobacterium Bacillus amyloliquefaciens SQR9 to Induce Plant Systemic Resistance and Their Interactions With Plant Signaling Pathways." Molecular Plant-Microbe Interactions® 31, no. 5 (May 2018): 560–67. http://dx.doi.org/10.1094/mpmi-11-17-0273-r.

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Beneficial rhizobacteria have been reported to produce various elicitors that induce plant systemic resistance, but there is little knowledge concerning the relative contribution of multiple elicitors from a single beneficial rhizobacterium on the induced systemic resistance in plants and the interactions of these elicitors with plant signaling pathways. In this study, nine mutants of the plant growth–promoting rhizobacterium Bacillus amyloliquefaciens SQR9 deficient in producing the extracellular compounds, including fengycin, bacillomycin D, surfactin, bacillaene, macrolactin, difficidin, bacilysin, 2,3-butandiol, and exopolysaccharides, were tested for the induction of systemic resistance against Pseudomonas syringae pv. tomato DC3000 and Botrytis cinerea and the transcription of the salicylic acid, jasmonic acid, and ethylene signaling pathways in Arabidopsis. Deficiency in producing any of these compounds in SQR9 significantly weakened the induced plant resistance against these phytopathogens. These SQR9-produced elicitors induced different plant defense genes. For instance, the enhancement of 1,3-glucanase (PR2) by SQR9 was impaired by a deficiency of macrolactin but not surfactin. SQR9 mutants deficient in the lipopeptide and polyketide antibiotics remained only 20% functional for the induction of resistance-related gene transcription. Overall, these elicitors of SQR9 could act synergistically to induce plant systemic resistance against different phytopathogens through different signaling pathway genes, and the bacterial antibiotics are major contributors to the induction.

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24

Van Wees, Saskia C. M., Corné M. J. Pieterse, Annemiek Trijssenaar, Yvonne A. M. Van 't Westende, Femke Hartog, and Leendert C. Van Loon. "Differential Induction of Systemic Resistance in Arabidopsis by Biocontrol Bacteria." Molecular Plant-Microbe Interactions® 10, no. 6 (August 1997): 716–24. http://dx.doi.org/10.1094/mpmi.1997.10.6.716.

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Selected nonpathogenic, root-colonizing bacteria are able to elicit induced systemic resistance (ISR) in plants. To elucidate the molecular mechanisms underlying this type of systemic resistance, an Arabidopsis-based model system was developed in which Pseudomonas syringae pv. tomato and Fusarium oxysporum f. sp. raphani were used as challenging pathogens. In Arabidopsis thaliana ecotypes Columbia and Landsberg erecta, colonization of the rhizosphere by P. fluorescens strain WCS417r induced systemic resistance against both pathogens. In contrast, ecotype RLD did not respond to WCS417r treatment, whereas all three ecotypes expressed systemic acquired resistance upon treatment with salicylic acid (SA). P. fluorescens strain WCS374r, previously shown to induce ISR in radish, did not elicit ISR in Arabidopsis. The opposite was found for P. putida strain WCS358r, which induced ISR in Arabidopsis but not in radish. These results demonstrate that rhizosphere pseudomonads are differentially active in eliciting ISR in related plant species. The outer membrane lipopolysaccharide (LPS) of WCS417r is the main ISR-inducing determinant in radish and carnation, and LPS-containing cell walls also elicit ISR in Arabidopsis. However, mutant WCS417rOA¯, lacking the O-antigenic side chain of the LPS, induced levels of protection similar to those induced by wild-type WCS417r. This indicates that ISR-inducing bacteria produce more than a single factor that trigger ISR in Arabidopsis. Furthermore, WCS417r and WCS358r induced protection in both wildtype Arabidopsis and SA-nonaccumulating NahG plants without activating pathogenesis-related gene expression. This suggests that elicitation of an SA-independent signaling pathway is a characteristic feature of ISR-inducing biocontrol bacteria.

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25

Jeun, Yong-Chull, Kyungseok Park, and Choong-Hoe Kim. "Different Mechanisms of Induced Systemic Resistance and Systemic Acquired Resistance AgainstColletotrichum orbiculareon the Leaves of Cucumber Plants." Mycobiology 29, no. 1 (March 2001): 19–26. http://dx.doi.org/10.1080/12298093.2001.12015756.

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26

Han, D. Y., D. L. Coplin, W. D. Bauer, and H. A. J. Hoitink. "A Rapid Bioassay for Screening Rhizosphere Microorganisms for Their Ability to Induce Systemic Resistance." Phytopathology® 90, no. 4 (April 2000): 327–32. http://dx.doi.org/10.1094/phyto.2000.90.4.327.

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We developed a rapid and miniaturized bioassay for screening large numbers of rhizosphere microorganisms for their ability to induce systemic resistance to bacterial leaf spot of radish caused by Xanthomonas campestris pv. armoraciae. In this bioassay, Pantoea agglomerans strain E278Ar controlled symptoms of disease as effectively as 2,6-dichloroisonicotinic acid when applied to the roots of seedlings produced in growth pouches in a soilless system. E278Ar essentially did not migrate from seedling roots to the foliage. This suggests that induction of systemic resistance could best explain the observed reduction in disease severity. Three mini-Tn5Km-induced mutants of strain E278Ar were isolated that had lost the ability to induce resistance. The bioassay also was used to demonstrate that the fungal biocontrol agent Trichoderma hamatum strain 382 induces systemic resistance in radish. The bioassay required only 14 to 18 days from seeding until rating for disease severity, which is 10 to 14 days less than earlier bioassays.

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27

Ran, L. X., L. C. van Loon, and P. A. H. M. Bakker. "No Role for Bacterially Produced Salicylic Acid in Rhizobacterial Induction of Systemic Resistance in Arabidopsis." Phytopathology® 95, no. 11 (November 2005): 1349–55. http://dx.doi.org/10.1094/phyto-95-1349.

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The role of bacterially produced salicylic acid (SA) in the induction of systemic resistance in plants by rhizobacteria is far from clear. The strong SA producer Pseudomonas fluorescens WCS374r induces resistance in radish but not in Arabidopsis thaliana, whereas application of SA leads to induction of resistance in both plant species. In this study, we compared P. fluorescens WCS374r with three other SA-producing fluorescent Pseudomonas strains, P. fluorescens WCS417r and CHA0r, and P. aeruginosa 7NSK2 for their abilities to produce SA under different growth conditions and to induce systemic resistance in A. thaliana against bacterial speck, caused by P. syringae pv. tomato. All strains produced SA in vitro, varying from 5 fg cell-1 for WCS417r to >25 fg cell-1 for WCS374r. Addition of 200 μM FeCl3 to standard succinate medium abolished SA production in all strains. Whereas the incubation temperature did not affect SA production by WCS417r and 7NSK2, strains WCS374r and CHA0r produced more SA when grown at 33 instead of 28°C. WCS417r, CHA0r, and 7NSK2 induced systemic resistance apparently associated with their ability to produce SA, but WCS374r did not. Conversely, a mutant of 7NSK2 unable to produce SA still triggered induced systemic resistance (ISR). The possible involvement of SA in the induction of resistance was evaluated using SA-nonaccumulating transgenic NahG plants. Strains WCS417r, CHA0r, and 7NSK2 induced resistance in NahG Arabidopsis. Also, WCS374r, when grown at 33 or 36°C, triggered ISR in these plants, but not in ethylene-insensitive ein2 or in non-plant pathogenesis- related protein-expressing npr1 mutant plants, irrespective of the growth temperature of the bacteria. These results demonstrate that, whereas WCS374r can be manipulated to trigger ISR in Arabidopsis, SA is not the primary determinant for the induction of systemic resistance against bacterial speck disease by this bacterium. Also, for the other SAproducing strains used in this study, bacterial determinants other than SA must be responsible for inducing resistance.

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28

HYAKUMACHI, Mitsuro. "Systemic Resistance in Plants Induced by Beneficial Rhizosphere Microorganisms." Journal of Pesticide Science 23, no. 4 (1998): 422–26. http://dx.doi.org/10.1584/jpestics.23.422.

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29

Davis, RD, JAG Irwin, and RK Shepherd. "Induced systemic resistance in Stylosanthes spp. to Colletotrichum gloeosporioides." Australian Journal of Agricultural Research 39, no. 3 (1988): 399. http://dx.doi.org/10.1071/ar9880399.

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Systemic resistance to anthracnose caused by Colletotrichum gloeosporioides was induced in Stylosanthes humilis cv. Paterson and S.guianensis cv. Endeavour plants by protection inoculation (PI) with sub-lethal amounts of C. gloeosporioides inoculum. The protection was demonstrated on leaves produced after the plants had first become infected. When challenged with inoculum, these leaves produced significantly less severe lesions than on corresponding leaves on non-protected plants. The induced resistance effect diminished with time on the youngest leaves of plants which were challenged up to 39 days from the PI. The experiments also showed that young Stylosanthes spp. leaves (up to seven days after first appearance) were more susceptible to anthracnose infections than older leaves. When leaves of S. humilis and S. guianensis were inoculated at 24 and 30 days after first appearance respectively, very few infections occurred. These two factors may help explain observed anthracnose occurrence patterns in Stylosanthes spp. pastures.

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30

Heller, Werner E., and Cesare Gessler. "Induced Systemic Resistance in Tomato Plants against Phytophthora infestans." Journal of Phytopathology 116, no. 4 (August 1986): 323–28. http://dx.doi.org/10.1111/j.1439-0434.1986.tb00927.x.

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31

Riera, Nadia, Han Wang, Yong Li, Jinyun Li, Kirsten Pelz-Stelinski, and Nian Wang. "Induced Systemic Resistance Against Citrus Canker Disease by Rhizobacteria." Phytopathology® 108, no. 9 (September 2018): 1038–45. http://dx.doi.org/10.1094/phyto-07-17-0244-r.

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Citrus canker, caused by Xanthomonas citri subsp. citri, is an important citrus disease that causes significant economic losses worldwide. All commercial citrus varieties are susceptible to citrus canker. Currently, chemical control with copper based products is the main approach to control X. citri subsp. citri dispersal and plant colonization. However, extensive use of copper compounds can result in copper-resistant strains and cause adverse effects on the environment. Alternatives to chemical control involve the activation of citrus immunity to control the disease. Here, we investigated the ability of multiple rhizobacteria to induce a systemic defense response in cultivar Duncan grapefruit. Burkholderia territorii strain A63, Burkholderia metallica strain A53, and Pseudomonas geniculata strain 95 were found to effectively activate plant defense and significantly reduce symptom development in leaves challenged with X. citri subsp. citri. In the priming phase, root application of P. geniculata induced the expression of salicylic acid (SA)-signaling pathway marker genes (PR1, PR2, PR5, and salicylic acid carboxyl methyltransferase [SAM-SACM]). Gene expression analyses after X. citri subsp. citri challenge showed that root inoculation with P. geniculata strain 95 increased the relative levels of phenylalanine ammonia lyase 1 and SAM-SACM, two genes involved in the phenylpropanoid pathway as well as the biosynthesis of SA and methyl salicylate (MeSA), respectively. However, hormone analyses by UPLC-MS/MS showed no significant difference between SA in P. geniculata-treated plants and control plants at 8 days post-beneficial bacteria root inoculation. Moreover, P. geniculata root-treated plants contained higher reactive oxygen species levels in aerial tissues than control plants 8 days post-treatment application. This study demonstrates that rhizobacteria can modulate citrus immunity resulting in a systemic defense response against X. citri subsp. citri under greenhouse conditions.

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32

Hoffland, Ellis. "Comparison of Systemic Resistance Induced by Avirulent and NonpathogenicPseudomonasSpecies." Phytopathology 86, no. 7 (1996): 757. http://dx.doi.org/10.1094/phyto-86-757.

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33

Verhagen, Bas W. M., Jane Glazebrook, Tong Zhu, Hur-Song Chang, L. C. van Loon, and Corné M. J. Pieterse. "The Transcriptome of Rhizobacteria-Induced Systemic Resistance in Arabidopsis." Molecular Plant-Microbe Interactions® 17, no. 8 (August 2004): 895–908. http://dx.doi.org/10.1094/mpmi.2004.17.8.895.

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Plants develop an enhanced defensive capacity against a broad spectrum of plant pathogens after colonization of the roots by selected strains of nonpathogenic, fluorescent Pseudomonas spp. In Arabidopsis thaliana, this rhizobacteria-induced systemic resistance (ISR) functions independently of salicylic acid but requires responsiveness to the plant hormones jasmonic acid and ethylene. In contrast to pathogen-induced systemic acquired resistance, rhizobacteria-mediated ISR is not associated with changes in the expression of genes encoding pathogenesis-related proteins. To identify ISR-related genes, we surveyed the transcriptional response of over 8,000 Arabidopsis genes during rhizobacteria-mediated ISR. Locally in the roots, ISR-inducing Pseudomonas fluorescens WCS417r bacteria elicited a substantial change in the expression of 97 genes. However, systemically in the leaves, none of the approximately 8,000 genes tested showed a consistent change in expression in response to effective colonization of the roots by WCS417r, indicating that the onset of ISR in the leaves is not associated with detectable changes in gene expression. After challenge inoculation of WCS417r-induced plants with the bacterial leaf pathogen P. syringae pv. tomato DC3000, 81 genes showed an augmented expression pattern in ISR-expressing leaves, suggesting that these genes were primed to respond faster or more strongly upon pathogen attack. The majority of the primed genes was predicted to be regulated by jasmonic acid or ethylene signaling. Priming of pathogen-induced genes allows the plant to react more effectively to the invader encountered, which might explain the broad-spectrum action of rhizobacteria-mediated ISR.

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Faoro, Franco, and Franco Gozzo. "Is modulating virus virulence by induced systemic resistance realistic?" Plant Science 234 (May 2015): 1–13. http://dx.doi.org/10.1016/j.plantsci.2015.01.011.

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Choudhary, Devendra K., Anil Prakash, and B. N. Johri. "Induced systemic resistance (ISR) in plants: mechanism of action." Indian Journal of Microbiology 47, no. 4 (December 2007): 289–97. http://dx.doi.org/10.1007/s12088-007-0054-2.

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Ahmad, Aqeel, Shazia Shafique, and Sobiya Shafique. "Intracellular interactions involved in induced systemic resistance in tomato." Scientia Horticulturae 176 (September 2014): 127–33. http://dx.doi.org/10.1016/j.scienta.2014.07.004.

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Park, K. S., D. Paul, J. S. Kim, and J. W. Park. "l-Alanine augments rhizobacteria-induced systemic resistance in cucumber." Folia Microbiologica 54, no. 4 (July 2009): 322–26. http://dx.doi.org/10.1007/s12223-009-0041-6.

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Salwan, Richa, Monika Sharma, Amit Sharma, and Vivek Sharma. "Insights into plant beneficial microorganism-triggered induced systemic resistance." Plant Stress 7 (March 2023): 100140. http://dx.doi.org/10.1016/j.stress.2023.100140.

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Seifi, Alireza. "Write 'systemic small RNAs': read 'systemic immunity'." Functional Plant Biology 38, no. 10 (2011): 747. http://dx.doi.org/10.1071/fp11100.

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About 50 years ago, it was reported that pathogen-infected plants are less susceptible to a broad spectrum of the subsequent pathogen attacks. This form of induced resistance, which resembles the immunisation in mammalian cells, is called systemic acquired resistance (SAR). In the last 10 years, plant molecular biology has been revolutionised by the discovery of RNA silencing, which is also a systemic phenomenon and also contributes to plant immunity. Here, I review these two systemic phenomena in a comparative way to highlight the possibility that systemic silencing contributes to systemic immunity. This potential contribution could be in the process of gene expression reprogramming, which is needed for SAR induction, and/or in SAR signal complex, and/or in establishing SAR in remote tissues and forming priming status.

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Bhavanam, Santhi, and Michael J. Stout. "Assessment of Silicon- and Mycorrhizae- Mediated Constitutive and Induced Systemic Resistance in Rice, Oryza sativa L., against the Fall Armyworm, Spodoptera frugiperda Smith." Plants 10, no. 10 (October 7, 2021): 2126. http://dx.doi.org/10.3390/plants10102126.

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Induced resistance provides protection in plants against insect herbivores. Silicon and mycorrhizae often prime plant defenses and thereby enhance plant resistance against herbivores. In rice, Oryza sativa L., insect injury has been shown to induce resistance against future defoliators. However, it is unknown if silicon and mycorrhizae treatments in combination with insect injury result in greater induced resistance. Using the fall armyworm (FAW), Spodoptera frugiperda Smith, two experiments were conducted to investigate whether (1) silicon or mycorrhizae treatment alters resistance in rice and (2) induced systemic resistance in response to insect injury is augmented in silicon- or mycorrhizae- treated plants. In the first experiment, silicon treatment reduced FAW growth by 20% while mycorrhizae increased FAW growth by 8%. In the second experiment, insect injury induced systemic resistance, resulting in a 23% reduction in FAW larval weight gains on injured compared to uninjured plants, irrespective of treatment. Neither silicon nor mycorrhizae enhanced this systemic resistance in insect-injured plants. Furthermore, mycorrhizae resulted in the systemic increase of peroxidase (POD) and polyphenol oxidase (PPO) activities, and injury caused a slight decrease in these enzyme activities in mycorrhizae plants. Silicon treatment did not result in a stronger induction of POD and PPO activity in injured plants. Taken together, these results indicate a lack of silicon and mycorrhizae priming of plant defenses in rice. Regardless of injury, silicon reduced FAW weight gains by 36%. Based on these results, it appears silicon-mediated biomechanical rather than biochemical defenses may play a greater role in increased resistance against FAW in rice.

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Dong, H., and S. V. Beer. "Riboflavin Induces Disease Resistance in Plants by Activating a Novel Signal Transduction Pathway." Phytopathology® 90, no. 8 (August 2000): 801–11. http://dx.doi.org/10.1094/phyto.2000.90.8.801.

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The role of riboflavin as an elicitor of systemic resistance and an activator of a novel signaling process in plants was demonstrated. Following treatment with riboflavin, Arabidopsis thaliana developed systemic resistance to Peronospora parasitica and Pseudomonas syringae pv. Tomato, and tobacco developed systemic resistance to Tobacco mosaic virus (TMV) and Alternaria alternata. Riboflavin, at concentrations necessary for resistance induction, did not cause cell death in plants or directly affect growth of the culturable pathogens. Riboflavin induced expression of pathogenesis-related (PR) genes in the plants, suggesting its ability to trigger a signal transduction pathway that leads to systemic resistance. Both the protein kinase inhibitor K252a and mutation in the NIM1/NPR1 gene which controls transcription of defense genes, impaired responsiveness to riboflavin. In contrast, riboflavin induced resistance and PR gene expression in NahG plants, which fail to accumulate salicylic acid (SA). Thus, riboflavin-induced resistance requires protein kinase signaling mechanisms and a functional NIM1/NPR1 gene, but not accumulation of SA. Riboflavin is an elicitor of systemic resistance, and it triggers resistance signal transduction in a distinct manner.

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Gupta, Rupali, Ravindran Keppanan, Meirav Leibman-Markus, Dalia Rav-David, Yigal Elad, Dana Ment, and Maya Bar. "The Entomopathogenic Fungi Metarhizium brunneum and Beauveria bassiana Promote Systemic Immunity and Confer Resistance to a Broad Range of Pests and Pathogens in Tomato." Phytopathology® 112, no. 4 (April 2022): 784–93. http://dx.doi.org/10.1094/phyto-08-21-0343-r.

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Biocontrol agents can control pathogens by reenforcing systemic plant resistance through systemic acquired resistance (SAR) or induced systemic resistance (ISR). Trichoderma spp. can activate the plant immune system through ISR, priming molecular mechanisms of defense against pathogens. Entomopathogenic fungi (EPF) can infect a wide range of arthropod pests and play an important role in reducing pests’ population. Here, we investigated the mechanisms by which EPF control plant diseases. We tested two well studied EPF, Metarhizium brunneum isolate Mb7 and Beauveria bassiana as the commercial product Velifer, for their ability to induce systemic immunity and disease resistance against several fungal and bacterial phytopathogens, and their ability to promote plant growth. We compared the activity of these EPF to an established biocontrol agent, Trichoderma harzianum T39, a known inducer of systemic plant immunity and broad disease resistance. The three fungal agents were effective against several fungal and bacterial plant pathogens and arthropod pests. Our results indicate that EPF induce systemic plant immunity and disease resistance by activating the plant host defense machinery, as evidenced by increases in reactive oxygen species production and defense gene expression, and that EPF promote plant growth. EPF should be considered as control means for Tuta absoluta. We demonstrate that, with some exceptions, biocontrol in tomato can be equally potent by the tested EPF and T. harzianum T39, against both insect pests and plant pathogens. Taken together, our findings suggest that EPF may find use in broad-spectrum pest and disease management and as plant growth promoting agents.

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Vidal, Sabina, Anders R. B. Eriksson, Marcos Montesano, Jürgen Denecke, and E. Tapio Palva. "Cell Wall-Degrading Enzymes from Erwinia carotovora Cooperate in the Salicylic Acid-Independent Induction of a Plant Defense Response." Molecular Plant-Microbe Interactions® 11, no. 1 (January 1998): 23–32. http://dx.doi.org/10.1094/mpmi.1998.11.1.23.

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The virulence of the plant pathogen Erwinia carotovora subsp. carotovora is dependent on the production and secretion of a large variety of plant cell wall-degrading enzymes, including several pectinases and cellulases. Treatment of tobacco plants with culture filtrates (CFs) from the pathogen (containing the secreted cell wall-degrading enzymes) induces both local and systemic expression of genes involved in plant defense response. We have characterized the contribution of individually produced cell wall-degrading enzymes from E. carotovora subsp. carotovora in their ability to trigger local and systemic induction of a defense-related gene (coding for a basic β-1,3-glucanase) as well as resistance to this pathogen in tobacco. Our results show that mainly pectic enzymes and to some extent one cellulase induce expression of the β-1,3-glucanase gene. Cellulases appear to act cooperatively in the defense gene induction when added in combination with pectic enzymes. Similarly, pectinases and cellulases cooperate in triggering systemic resistance to the pathogen. Salicylic acid (SA) does not appear to be involved in this process, as systemic resistance was induced similarly in transgenic NahG plants that overproduce a salicylate hydroxylase and cannot accumulate SA and in nontrans-formed control plants. The lack of SA requirement for the induced resistance against E. carotovora subsp. carotovora suggests the presence of a different signal transduction pathway involved in this plant-pathogen interaction.

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Eschen-Lippold, Lennart, Simone Altmann, and Sabine Rosahl. "dl-β-Aminobutyric Acid–Induced Resistance of Potato Against Phytophthora infestans Requires Salicylic Acid but Not Oxylipins." Molecular Plant-Microbe Interactions® 23, no. 5 (May 2010): 585–92. http://dx.doi.org/10.1094/mpmi-23-5-0585.

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Inducing systemic resistance responses in crop plants is a promising alternative way of disease management. To understand the underlying signaling events leading to induced resistance, functional analyses of plants defective in defined signaling pathway steps are required. We used potato, one of the economically most-important crop plants worldwide, to examine systemic resistance against the devastating late blight pathogen Phytophthora infestans, induced by treatment with dl-β-aminobutyric acid (BABA). Transgenic plants impaired in either the 9-lipoxygenase pathway, which produces defense-related compounds, or the 13-lipoxygenase pathway, which generates jasmonic acid–derived signals, expressed wild-type levels of BABA-induced resistance. Plants incapable of accumulating salicylic acid (SA), on the other hand, failed to mount this type of induced resistance. Consistently, treatment of these plants with the SA analog 2,6-dichloroisonicotinic acid restored BABA-induced resistance. Together, these results demonstrate the indispensability of a functional SA pathway for systemic resistance in potato induced by BABA.

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Zhuang, Xia, Jian-Long Zhao, Miao Bai, Xing-Xing Ping, Yan-Lin Li, Yu-Hong Yang, Zhen-Chuan Mao, Guo-Shun Yang, and Bing-Yan Xie. "Pochonia chlamydosporia Isolate PC-170-Induced Expression of Marker Genes for Defense Pathways in Tomatoes Challenged by Different Pathogens." Microorganisms 9, no. 9 (September 5, 2021): 1882. http://dx.doi.org/10.3390/microorganisms9091882.

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Pochonia chlamydosporia is a fungal parasite of nematode eggs. Studies have shown that some strains of Pochonia chlamydosporia can promote plant growth and induce plants’ systemic resistance to root-knot nematodes by colonizing in their roots. This study aimed to verify the effect of the PC-170 strain on tomato growth and systemic resistance. Split-root experiments were conducted to observe the systemic resistance induced by PC-170. To explore the defense pathway that was excited due to the colonization by PC-170, we tested the expression of marker genes for defense pathways, and used mutant lines to verify the role of plant defense pathways. Our results showed that PC-170 can colonize roots, and promotes growth. We found a role for jasmonic acid (JA) in modulating tomato colonization by PC-170. PC-170 can activate tomato defense responses to reduce susceptibility to infection by the root-knot nematode Meloidogyne incognita, and induced resistance to some pathogens in tomatoes. The marker genes of the defense pathway were significantly induced after PC-170 colonization. However, salicylic acid (SA)- and jasmonic acid (JA)-dependent defenses in roots were variable with the invasion of different pathogens. Defense pathways play different roles at different points in time. SA- and JA-dependent defense pathways were shown to cross-communicate. Different phytohormones have been involved in tomato plants’ responses against different pathogens. Our study confirmed that adaptive JA signaling is necessary to regulate PC-170 colonization and induce systemic resistance in tomatoes.

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Ryu, Hojin. "Enhancing resistance to major fungal pathogens ofPanax ginseng, by BTH-induced systemic resistance." Journal of Plant Biotechnology 43, no. 1 (March 31, 2016): 99–103. http://dx.doi.org/10.5010/jpb.2016.43.1.99.

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Kusajima, Miyuki, Moeka Fujita, Khamsalath Soudthedlath, Hidemitsu Nakamura, Koichi Yoneyama, Takahito Nomura, Kohki Akiyama, Akiko Maruyama-Nakashita, Tadao Asami, and Hideo Nakashita. "Strigolactones Modulate Salicylic Acid-Mediated Disease Resistance in Arabidopsis thaliana." International Journal of Molecular Sciences 23, no. 9 (May 8, 2022): 5246. http://dx.doi.org/10.3390/ijms23095246.

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Strigolactones are low-molecular-weight phytohormones that play several roles in plants, such as regulation of shoot branching and interactions with arbuscular mycorrhizal fungi and parasitic weeds. Recently, strigolactones have been shown to be involved in plant responses to abiotic and biotic stress conditions. Herein, we analyzed the effects of strigolactones on systemic acquired resistance induced through salicylic acid-mediated signaling. We observed that the systemic acquired resistance inducer enhanced disease resistance in strigolactone-signaling and biosynthesis-deficient mutants. However, the amount of endogenous salicylic acid and the expression levels of salicylic acid-responsive genes were lower in strigolactone signaling-deficient max2 mutants than in wildtype plants. In both the wildtype and strigolactone biosynthesis-deficient mutants, the strigolactone analog GR24 enhanced disease resistance, whereas treatment with a strigolactone biosynthesis inhibitor suppressed disease resistance in the wildtype. Before inoculation of wildtype plants with pathogenic bacteria, treatment with GR24 did not induce defense-related genes; however, salicylic acid-responsive defense genes were rapidly induced after pathogenic infection. These findings suggest that strigolactones have a priming effect on Arabidopsis thaliana by inducing salicylic acid-mediated disease resistance.

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Reitz, M., K. Rudolph, I. Schröder, S. Hoffmann-Hergarten, J. Hallmann, and R. A. Sikora. "Lipopolysaccharides of Rhizobium etliStrain G12 Act in Potato Roots as an Inducing Agent of Systemic Resistance to Infection by the Cyst Nematode Globodera pallida." Applied and Environmental Microbiology 66, no. 8 (August 1, 2000): 3515–18. http://dx.doi.org/10.1128/aem.66.8.3515-3518.2000.

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ABSTRACT Recent studies have shown that living and heat-killed cells of the rhizobacterium Rhizobium etli strain G12 induce in potato roots systemic resistance to infection by the potato cyst nematodeGlobodera pallida. To better understand the mechanisms of induced resistance, we focused on identifying the inducing agent. Since heat-stable bacterial surface carbohydrates such as exopolysaccharides (EPS) and lipopolysaccharides (LPS) are essential for recognition in the symbiotic interaction betweenRhizobium and legumes, their role in the R. etli-potato interaction was studied. EPS and LPS were extracted from bacterial cultures, applied to potato roots, and tested for activity as an inducer of plant resistance to the plant-parasitic nematode. Whereas EPS did not affect G. pallida infection, LPS reduced nematode infection significantly in concentrations as low as 1 and 0.1 mg ml−1. Split-root experiments, guaranteeing a spatial separation of inducing agent and challenging pathogen, showed that soil treatments of one half of the root system with LPS resulted in a highly significant (up to 37%) systemic induced reduction ofG. pallida infection of potato roots in the other half. The results clearly showed that LPS of R. etli G12 act as the inducing agent of systemic resistance in potato roots.

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Cyphert, Travis J., Robert T. Morris, Lawrence M. House, Tammy M. Barnes, Yolanda F. Otero, Whitney J. Barham, Raphael P. Hunt, et al. "NF-κB-dependent airway inflammation triggers systemic insulin resistance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 9 (November 1, 2015): R1144—R1152. http://dx.doi.org/10.1152/ajpregu.00442.2014.

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Inflammatory lung diseases (e.g., pneumonia and acute respiratory distress syndrome) are associated with hyperglycemia, even in patients without a prior diagnosis of Type 2 diabetes. It is unknown whether the lung inflammation itself or the accompanying comorbidities contribute to the increased risk of hyperglycemia and insulin resistance. To investigate whether inflammatory signaling by airway epithelial cells can induce systemic insulin resistance, we used a line of doxycycline-inducible transgenic mice that express a constitutive activator of the NF-κB in airway epithelial cells. Airway inflammation with accompanying neutrophilic infiltration was induced with doxycycline over 5 days. Then, hyperinsulinemic-euglycemic clamps were performed in chronically catheterized, conscious mice to assess insulin action. Lung inflammation decreased the whole body glucose requirements and was associated with secondary activation of inflammation in multiple tissues. Metabolic changes occurred in the absence of hypoxemia. Lung inflammation markedly attenuated insulin-induced suppression of hepatic glucose production and moderately impaired insulin action in peripheral tissues. The hepatic Akt signaling pathway was intact, while hepatic markers of inflammation and plasma lactate were increased. As insulin signaling was intact, the inability of insulin to suppress glucose production in the liver could have been driven by the increase in lactate, which is a substrate for gluconeogenesis, or due to an inflammation-driven signal that is independent of Akt. Thus, localized airway inflammation that is observed during inflammatory lung diseases can contribute to systemic inflammation and insulin resistance.

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Mizutani, Shigetoshi, Masahiro Endo, Toshiaki Ino-ue, Masahiro Kurasawa, Yoko Uno, Hideharu Saito, Kaoru Onogi, Ikunoshin Kato, and Kazutoh Takesako. "CD4+-T-Cell-Mediated Resistance to Systemic Murine Candidiasis Induced by a Membrane Fraction ofCandida albicans." Antimicrobial Agents and Chemotherapy 44, no. 10 (October 1, 2000): 2653–58. http://dx.doi.org/10.1128/aac.44.10.2653-2658.2000.

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ABSTRACT We induced resistance to systemic Candida albicansinfection through CD4+-cell-mediated immunity in mice by immunization with subcutaneous injections of live C. albicans cells emulsified in incomplete Freund adjuvant. Using the resistant mice, we tested subcellular fractions of C. albicans cells for antigenicity. The fractions were derived from digested surface cell walls, insoluble membranes, or soluble and insoluble cytoplasmic materials, which were prepared by treatment with cell wall-digesting enzymes followed by lysis of the consequent protoplasts. Interestingly, the live-cell-immunized mice showed strong cell-mediated immune responses to the membrane fraction (C. albicans membrane antigen [CMA]). In addition, immunization with CMA induced resistance to systemic candidiasis, which disappeared upon administration of anti-CD4 monoclonal antibody. Infusion of splenocytes from the CMA-immunized mice conferred resistance on SCID mice, whereas infusion of CD4+-T-cell-depleted splenocytes was unable to induce resistance, indicating the importance of CD4+ lymphocytes for resistance. These results suggest a potential for the membrane fraction to act as an antigen conferring resistance to systemic candidiasis in place of live cells and also as a source for the isolation of a new antigen.

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