Molecular Pathogens 2024, Vol.15, No.1, 30-39 http://microbescipublisher.com/index.php/mp 35 Overexpressing the transcription factors PalbHLH1 and PalMYB90 in poplar trees significantly enhances the plants' disease resistance, primarily by increasing the content of flavonoid compounds. These compounds include total phenols, proanthocyanidins (PAs), anthocyanins, and the intermediate products quercetin and kaempferol. Transgenic poplars exhibit enhanced antioxidant enzyme activity and hydrogen peroxide release when facing infections fromBotrytis cinerea and Dothiorella gregaria, changes that are associated with the upregulation of key genes in the flavonoid metabolic pathway. Specifically, transcriptomic analysis shows that, following pathogen infection, genes related to the flavonoid biosynthesis pathway, such as PalF3H, PalDFR, PalANS, and PalANR, are significantly upregulated in poplars overexpressing PalbHLH1 and PalMYB90. These genes play critical roles in the initial, intermediate, and final steps of anthocyanin and proanthocyanidin synthesis. These findings suggest that flavonoid compounds play an important role in plant defense mechanisms, and a similar mechanism may exist in tea trees. Additionally, the metabolic pathways for flavonoid biosynthesis are enriched in resistant tea plant resources, further supporting their role in pathogen defense (Zhang et al., 2022). Tannins, which are a type of phenolic compound, also contribute to the structural defense by reinforcing cell walls and inhibiting pathogen growth (Wink et al., 2012). 5.3 Metabolic engineering for enhanced resistance Metabolic engineering offers a promising approach to enhance the resistance of tea plants by manipulating the biosynthetic pathways of secondary metabolites. For instance, the overexpression of CsHCT genes can be used to increase the production of phenolic acids and lignin, thereby improving resistance to both biotic and abiotic stresses (Chen et al., 2021). Similarly, engineering the flavonoid biosynthesis pathway by overexpressing key transcription factors can enhance the accumulation of flavonoids and improve pathogen resistance (Bai et al., 2020). Additionally, understanding the role of specific metabolites, such as anthocyanin-3-O-galactosides, in disease resistance can guide the development of resistant tea plant varieties through targeted metabolic engineering (Li et al., 2023). 6 Molecular Interactions Between Tea Plants and Pathogens 6.1 Pathogen effectors and host targets Pathogen effectors are molecules secreted by pathogens that manipulate host cell structure and function to facilitate infection and suppress host defense mechanisms. In tea plants, these effectors are recognized by specific resistance (R) genes, which encode proteins that detect the presence of pathogen-derived molecules. The interaction between pathogen effectors and host targets is a critical aspect of the plant's immune response. The meta-analysis by Kourelis and Hoorn (2018) identifies nine distinct mechanisms by which R proteins can trigger disease resistance, including both direct and indirect perception of pathogen molecules. 6.2 Host defense responses Upon recognition of pathogen effectors, tea plants activate a series of defense responses to combat the infection. These responses include the production of antimicrobial compounds, the strengthening of cell walls, and the activation of signaling pathways that lead to systemic acquired resistance (SAR). The transcriptome analysis by Jayaswall et al. (2016) reveals that tea plants express a variety of defense-related genes, including those encoding for defense enzymes, resistance genes, and transcription factors, in response to blister blight disease. Furthermore, the review by Zhang et al. (2013) discusses the two-tiered immune system in plants, comprising pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI), which collectively enhance the plant's ability to resist pathogen invasion. 6.3 Molecular arms race The interaction between tea plants and pathogens is characterized by a continuous molecular arms race, where both the host and the pathogen evolve new strategies to outcompete each other. Pathogens evolve new effectors to overcome plant defenses, while plants, in turn, develop new R genes to recognize these effectors. This
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