High temperature and high light intensity induced photoinhibition of bayberry (Myrica rubra Sieb. et Zucc.) by disruption of D1 turnover in photosystem II.

Highlights • High temperature and high light intensity induced bayberry photoinhibition. • D1 protein, Deg and FtsH proteases were destroyed by these stresses. • Photosystem II dysfunction was the main cause of photoinhibition. • Bayberry cultivar 'Dongkui' was more resistant to these stresses than 'Tanmei'. Abstract High temperature and high light intensity have negative effects on photosynthetic capacity. Bayberry (Myrica rubra Sieb. et Zucc.) photosynthesis is prone to decline under these stresses; however, the mechanisms underlying the low capacity of bayberry photosynthesis induced by these stresses remain largely unknown. The responses of two bayberry cultivars, 'Dongkui' and 'Tanmei', to stress were studied. At the optimum temperature (25 °C), high light intensity of 1500 μmol m−2s−1 (HL1500) strikingly decreased the values of effective quantum yield of photosystem II (Φ PS II), maximal quantum yield of PS II, photochemical quenching, and induced increases in non-photochemical quenching compared to the values of these fluorescence parameters at low light intensity of 500 μmol m−2s−1, while medium light intensity had less effect. Combining high temperature of 40 °C (HT40) and high light intensities (HL1500) enhanced this negative effect. Thus, both HT40 and HL1500 induced bayberry photoinhibition. Changes in the amounts of D1 protein and the proteases Deg1 and FtsH, as well as inhibitor experiments, suggested that D1 turnover was disrupted by both HT40 and HL1500. Analysis of the physiological changes in response to the above stresses implied that 'Dongkui' was more resistant than 'Tanmei' to both HT40 and HL1500. [ABSTRACT FROM AUTHOR]