CsPRR7 negatively regulates cold tolerance by repressing CsCBF3 in tea plants
Jie Wang1,2, Yongheng Zhang1,2, Yedie Wu1,2
1Key Laboratory of Biology, Genetics and Breeding of Special Economic Animals and Plants, Ministry of Agriculture and Rural Affairs, National Center for Tea Plant Improvement, Tea Research Institute, Chinese Academy of Agricultural Sciences, Hangzhou, 310008, Zhejiang, China.
Key Message:
CsPRR7 acts as a negative regulator of cold tolerance in tea plants via a CBF-dependent pathway. Low temperatures have caused severe damage to the growth and development of tea plants, directly impacting the quality and profitability of spring tea. Circadian clock plays an important role in sensing external environmental signals such as light and temperature, predicting daily environmental changes, and ensuring the rhythms of plant metabolism, physiology, and development. The PSEUDO RESPONSE REGULATOR (PRR) genes, key components of the circadian clock, play a vital role in plant adaptation to diurnal temperature changes. However, the specific role of the CsPRRs in tea plants in response to low-temperature stress, as well as the molecular regulatory mechanisms underlying this response, remain unclear. In this study, we characterized CsPRR7, a key component of the tea plant circadian oscillator, to explore its potential role in cold stress responses. The expression of CsPRR7 exhibits a distinct circadian rhythm. Furthermore, CsPRR7 was suppressed by low temperatures, and its rhythmic expression was significantly disrupted by cold stress treatment. Transient silencing of CsPRR7 enhanced cold tolerance in tea leaves, while its overexpression led to decreased cold tolerance. The yeast one-hybrid (Y1H) and dual-luciferase assays demonstrated that CsPRR7 inhibits the transcription of CsCBF3, a member of the C-repeat (CRT)/dehydration-responsive element (DRE)-binding factor (CBF) family, by directly binding to its promoter region. These results reveal that CsPRR7 acts as a negative regulator of cold tolerance in tea plants via a CBF-dependent pathway.
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