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Drought stress (DS) is the most important abiotic stress affecting yield and quality of tea worldwide. DS causes oxidative stress to cells due to the accumulation of reactive oxygen species (ROS). As non-enzymatic antioxidants, tea catechins can scavenge excess ROS in response to DS. Further, catechin accumulation contributes to the formation of oxidative polymerization products (e.g. theaflavins and thearubigins) that improve the quality of black tea. However, there are no systematic reports on the response of tea catechins to DS. First, we reviewed the available literature on the response of tea plants to DS. Second, we summarized the current knowledge of ROS production in tea leaves under DS and typical antioxidant response mechanisms. Third, we conducted a detailed review of the changes in catechin levels in tea under different drought conditions. We found that the total amounts of catechin and o-quinone increased under DS conditions. We propose that the possible mechanisms underlying tea catechin accumulation under DS conditions include (i) autotrophic formation of o-quinone, (ii) polymerization of proanthocyanidins that directly scavenge excess ROS, and (iii) formation of metal ion complexes and by influencing the antioxidant systems that indirectly eliminate excess ROS. Finally, we discuss ways of potentially improving black tea quality using drought before picking in the summer/fall dry season. In summary, we mainly discuss the antioxidant mechanisms of tea catechins under DS and the possibility of using drought to improve black tea quality. Our review provides a theoretical basis for the production of high-quality black tea under DS conditions.

Cellular homeostasis requires tight coordination between nucleus and mitochondria, organelles that each possesses their own genomes. Disrupted mitonuclear communication has been found to be implicated in many aging processes. However, little is known about mitonuclear signaling regulator in sarcopenia which is a major contributor to the risk of poor health‐related quality of life, disability, and premature death in older people. High‐temperature requirement protein A2 (HtrA2/Omi) is a mitochondrial protease and plays an important role in mitochondrial proteostasis. HtrA2mnd2(−/−) mice harboring protease‐deficient HtrA2/Omi Ser276Cys missense mutants exhibit premature aging phenotype. Additionally, HtrA2/Omi has been established as a signaling regulator in nervous system and tumors. We therefore asked whether HtrA2/Omi participates in mitonuclear signaling regulation in muscle degeneration. Using motor functional, histological, and molecular biological methods, we characterized the phenotype of HtrA2mnd2(−/−) muscle. Furthermore, we isolated the gastrocnemius muscle of HtrA2mnd2(−/−) mice and determined expression of genes in mitochondrial unfolded protein response (UPRmt), mitohormesis, electron transport chain (ETC), and mitochondrial biogenesis. Here, we showed that HtrA2/Omi protease deficiency induced denervation‐independent skeletal muscle degeneration with sarcopenia phenotypes. Despite mitochondrial hypofunction, upregulation of UPRmt and mitohormesis‐related genes and elevated total reactive oxygen species (ROS) production were not observed in HtrA2mnd2(−/−) mice, contrary to previous assumptions that loss of protease activity of HtrA2/Omi would lead to mitochondrial dysfunction as a result of proteostasis disturbance and ROS burst. Instead, we showed that HtrA2/Omi protease deficiency results in different changes between the expression of nuclear DNA‐ and mitochondrial DNA‐encoded ETC subunits, which is in consistent with their transcription factors, nuclear respiratory factors 1 and 2, and coactivator peroxisome proliferator‐activated receptor γ coactivator 1α. These results reveal that loss of HtrA2/Omi protease activity induces mitonuclear imbalance via differential regulation of mitochondrial biogenesis in sarcopenia. The novel mechanistic insights may be of importance in developing new therapeutic strategies for sarcopenia.

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