Experiment identifies decline in photosynthesis and increased oxidative stress during leaf senescence in Cunninghamia lanceolata seedlings, indicating carbon starvation.
Low inner leaves in the thick canopy of dense Chinese fir plantations frequently show premature senescence and dieback regardless of age. To elucidate the underlying mechanisms, a 28-day growth chamber experiment was conducted under dark conditions to induce leaf senescence. Changes in leaf area, photosynthetic performance, and the responses of carbon metabolism and the antioxidant defense system were analyzed. Leaf area decreased significantly with time in darkness. The photosystem Ⅱ reaction center was damaged, and fluorescence parameters and chlorophyll contents decreased, resulting in reduced light energy capture and conversion efficiencies. Photosynthetic rate, apparent quantum yield, stomatal conductance, transpiration rate, and light use efficiency all decreased, while the light compensation point and intercellular CO2 concentration increased. Antioxidant enzyme activities initially increased but eventually collapsed as the stress continued and H2O2 and malondialdehyde accumulated, causing membrane conductivity, i.e., membrane permeability, to increase by 122%. Meanwhile, reduced non-structural carbohydrates, especially total non-structural carbohydrates content, decreased by 45.32%, triggering sugar starvation and accelerating aging. Our study provided new physiological evidence for light-stress response mechanisms in Chinese fir. Specifically, it revealed that dark-induced leaf senescence was mainly caused by irreversible damage to the photosynthetic apparatus and oxidative stress, which together led to carbon starvation and ultimately death.
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Huang et al. (2025) studied this question.
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