Journal of Tea Science Research, 2025, Vol.15, No.1, 38-46 http://hortherbpublisher.com/index.php/jtsr 39 provide molecular tools for improvement through marker-assisted selection, genomic selection, and transgenic or genome editing technologies. Furthermore, understanding of stress-responsive genes and regulation networks will also be useful in developing sustainable cultivation strategies that are in conformity with climatic resilience and ecological balance (Li et al., 2025). This study presents a comprehensive overview of recent advances in the dissection of the genetics underlying tea plant stress tolerance. We provide molecular underpinnings of primary abiotic (drought, cold, salinity) and biotic (pathogens and pests) stress responses, describe key stress-responsive genes, transcription factors, and hormonal signaling pathways, and outline advances achieved through multi-omics approaches. Apart from this, future prospects of integrative strategies such as systems biology, genome editing, and molecular breeding are evaluated in terms of improving tea stress resistance. Opportunities and challenges are also shown, keeping in mind the aim of providing visions on future research directions and applications for sustainable tea production and industry growth. 2 Major Stress Factors and Physiological Responses in Tea Plants 2.1 Drought stress and osmotic adjustment mechanisms Drought is the most restrictive factor in tea production, with decreased water content, altered photosynthesis, and increased oxidative damage. The tea plants respond by synthesizing osmoprotectants such as proline and soluble carbohydrates, inducing antioxidant enzyme activity (e.g., superoxide dismutase, catalase, peroxidase), and activating abscisic acid (ABA) signaling and flavonoid biosynthesis genes. These activities help to maintain cell turgor, protect cellular constituents, and detoxify ROS under drought stress. Exogenous treatments like fulvic acid, ABA, and potassium also enhance drought tolerance by modulating these activities and enhancing antioxidant defense (Chaeikar et al., 2020; Gu et al., 2020; Sun et al., 2020; Zhang et al., 2020). 2.2 Cold Stress and adaptation to low temperature Cold stress suppresses photosynthetic process and induces ROS accumulation, resulting in cell injury. Tea plants react through the activation of antioxidant mechanisms, compatible solute accumulation, and induction of cold-inducible genes such as CBFs, ICE1, and dehydrins. Volatile organic compounds, including eugenol and (Z)-3-hexenol, also play signaling roles, inducing cold tolerance through ABA homeostasis and ROS scavenging. Such characteristics provide stability to membranes and retard leaf senescence under cold stress (Samarina et al., 2020; 2023) (Figure 1). 2.3 Salt stress and ionic homeostasis regulation Salt stress triggers ion imbalance and oxidative stress in tea leaves. Ionic homeostasis, especially by selective uptake and compartmentalization of Na+ and K+ ions, is necessary. Antioxidant defense and osmolyte accumulation (such as proline and sugars) are also activated to prevent salt-mediated injury. Plant growth-promoting bacteria also enhance salt tolerance by regulating ion transport and stress signaling (Li et al., 2019; Gamalero and Glick, 2022). 2.4 Biotic stress: disease, pest resistance, and plant immune responses Tea plants are attacked by various pathogens and insects, which trigger immunological responses by the induction of pathogenesis-related proteins, secondary metabolites (flavonoids and lignin), and hormone signaling mechanisms (salicylic acid and jasmonic acid). Drought stress and salt stress could increase biotic vulnerability but cross-protection can be elicited by beneficial microbes and the augmentation of antioxidant defense (Gamalero and Glick, 2022). 2.5 Combined effects of multiple stresses and interactive mechanisms Tea plants are typically exposed to combined stresses, e.g., cold and drought, triggering specific and general molecular responses. Transcriptome profiling indicates that combined stresses lead to unique patterns of gene expression, with crosstalk between ABA-dependent and -independent signaling pathways, and regulation of
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