Induction of pathogen resistance and pathogenesis-related genes in tobacco by a heat-stable Trichoderma mycelial extract and plant signal messengers

Anthracnose, caused by Colletotrichum gloeosporioides, is one of the most damaging pepper (Capsicum annum L.) disease. Melatonin induces transcription of defense-related genes that enhance resistance to pathogens and mediate physiological activities in plants. To study whether the melatonin-mediated pathogen resistance is associated with chitinase gene (CaChiIII2), pepper plants and Arabidopsis seeds were treated with melatonin, then CaChiIII2 activation, hydrogen peroxide (H2O2) levels, and antioxidant enzymes activity during plant–pathogen interactions were investigated. Melatonin pretreatment uncoupled the knockdown of CaChiIII2 and transiently activated its expression level in both control and CaChiIII2-silenced pepper plants and enhanced plant resistance. Suppression of CaChiIII2 in pepper plants showed a significant decreased in the induction of defense-related genes and resistance to pathogens compared with control plants. Moreover, melatonin efficiently enabled plants to maintain intracellular H2O2 concentrations at steady-state levels and enhanced the activities of antioxidant enzymes, which possibly improved disease resistance. The activation of the chitinase gene CaChiIII2 in transgenic Arabidopsis lines was elevated under C. gloeosporioides infection and exhibited resistance through decreasing H2O2 biosynthesis and maintaining H2O2 at a steady-state level. Whereas melatonin primed CaChiIII2-overexpressed (OE) and wild-type (WT) Arabidopsis seedlings displayed a remarkable increase in root-length compared to the unprimed WT plants. Using an array of CaChiIII2 knockdown and OE, we found that melatonin efficiently induced CaChiIII2 and other pathogenesis-related genes expressions, responsible for the innate immunity response of pepper against anthracnose disease.

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Host-Pathogen Interactions XXXIX. A Soybean Pathogenesis-Related Protein withβ-1,3-Glucanase Activity Releases Phytoalexin Elicitor-Active Heat-Stable Fragments from Fungal Walls

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-4-545 ◽

1991 ◽

Vol 4 (6) ◽

pp. 545 ◽

Cited By ~ 78

Author(s):

Kyung-Sik Ham

Keyword(s):

Related Protein ◽

Host Pathogen Interactions ◽

Glucanase Activity ◽

Heat Stable ◽

Pathogenesis Related Protein ◽

Pathogenesis Related ◽

Host Pathogen

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Ascorbic Acid Deficiency in Arabidopsis Induces Constitutive Priming That is Dependent on Hydrogen Peroxide, Salicylic Acid, and the NPR1 Gene

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-3-0340 ◽

2010 ◽

Vol 23 (3) ◽

pp. 340-351 ◽

Cited By ~ 67

Author(s):

Madhumati Mukherjee ◽

Katherine E. Larrimore ◽

Naushin J. Ahmed ◽

Tyler S. Bedick ◽

Nadia T. Barghouthi ◽

...

Keyword(s):

Ascorbic Acid ◽

Salicylic Acid ◽

Disease Resistance ◽

Pseudomonas Syringae ◽

Messenger Rna ◽

Bacterial Pathogen ◽

Pathogen Resistance ◽

Wild Type ◽

Pr Genes ◽

Pathogenesis Related

The ascorbic acid (AA)-deficient Arabidopsis thaliana vtc1-1 mutant exhibits increased resistance to the virulent bacterial pathogen Pseudomonas syringae. This response correlates with heightened levels of salicylic acid (SA), which induces antimicrobial pathogenesis-related (PR) proteins. To determine if SA-mediated, enhanced disease resistance is a general phenomenon of AA deficiency, to elucidate the signal that stimulates SA synthesis, and to identify the biosynthetic pathway through which SA accumulates, we studied the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants. We also studied double mutants defective in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H2O2, SA, and messenger RNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared with the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5, and NPR1 for SA biosynthesis and pathogen resistance. We suggest that AA deficiency causes constitutive priming through a buildup of H2O2 that stimulates SA accumulation, conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might be sensitized to H2O2 and SA production after infection.

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Naringenin Induces Pathogen Resistance Against Pseudomonas syringae Through the Activation of NPR1 in Arabidopsis

Frontiers in Plant Science ◽

10.3389/fpls.2021.672552 ◽

2021 ◽

Vol 12 ◽

Author(s):

Jonguk An ◽

Sun Ho Kim ◽

Sunghwa Bahk ◽

Uyen Thi Vuong ◽

Nhan Thi Nguyen ◽

...

Keyword(s):

Gene Expression ◽

Pseudomonas Syringae ◽

Nuclear Translocation ◽

Mek Inhibitor ◽

Pathogen Resistance ◽

Flavonoid Biosynthesis ◽

Transcriptional Coactivator ◽

Transcript Levels ◽

Physiological Processes ◽

Pathogenesis Related

Flavonoids are well known for the coloration of plant organs to protect UV and ROS and to attract pollinators as well. Flavonoids also play roles in many aspects of physiological processes including pathogen resistance. However, the molecular mechanism to explain how flavonoids play roles in pathogen resistance was not extensively studied. In this study, we investigated how naringenin, the first intermediate molecule of the flavonoid biosynthesis, functions as an activator of pathogen resistances. The transcript levels of two pathogenesis-related (PR) genes were increased by the treatment with naringenin in Arabidopsis. Interestingly, we found that naringenin triggers the monomerization and nuclear translocation of non-expressor of pathogenesis-related genes 1 (NPR1) that is a transcriptional coactivator of PR gene expression. Naringenin can induce the accumulation of salicylic acid (SA) that is required for the monomerization of NPR1. Furthermore, naringenin activates MPK6 and MPK3 in ROS-dependent, but SA-independent manners. By using a MEK inhibitor, we showed that the activation of a MAPK cascade by naringenin is also required for the monomerization of NPR1. These results suggest that the pathogen resistance by naringenin is mediated by the MAPK- and SA-dependent activation of NPR1 in Arabidopsis.

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