Transcriptome-based investigation of the response and repair mechanisms in the photosynthetic system of Cycas panzhihuaensis under dual high-temperature and drought stress

Abstract Background Cycas panzhihuaensis, as a national first-class protected plant, has long been threatened by dual high-temperature and drought stress. Photosynthesis is a key target of dual high-temperature and drought stress. However, the specific processes underlying post-injury recovery remain poorly characterized. Utilizing chlorophyll fluorescence parameters, chloroplast ultrastructure and transcriptome sequencing techniques, this investigation analyzes the photosynthetic damage of C. panzhihuaensis under dual high-temperature and drought stress and the repair mechanism of photosynthetic system after rehydration. Results The results showed that the maximum quantum yield of photosystem II decreased by 51.2% compared with the CK., the thylakoid structure disintegrated, the osmiophilic particles increased sharply, and the photosynthetic function was seriously damaged under the combined stress. Key genetic components responsible for the function of Photosystem I and II, ATP synthase and multiple photosynthesis-related transcription factors NAC, bHLH, WRKY, MYB, and ERF were synergistically down-regulated. Rewatering repair showed a sequential strategy of ' rapid water absorption → light protection priority → structural reconstruction ': when rewatering for 3 days, the leaf relative water content showed ' overcompensation '—a transient excess water uptake beyond the pre-stress level, but the photosynthetic function was further deteriorated, and the light protection mechanism was preferentially activated; after 7 days of rewatering, the grana thylakoids overlapped, osmiophilic particles decreased, the maximum quantum yield recovered to 0.689, the core photosystem genes and transcription factors were up-regulated, and the photosynthetic function was partially restored. A key observation was the delayed recovery of the LHCB gene family, particularly LHCB1 and LHCB2 homologs.