Exploring LHCSR3 expression and its role in Chlamydomonas reinhardtii under osmotic stress: Implications for non-photochemical quenching mechanism

Plants have a protective mechanism called non-photochemical quenching to prevent damage caused by excessive sunlight. A critical component of this mechanism is energy-dependent quenching (qE). In Chlamydomonas reinhardtii, the protein expression called light-harvesting complex stress-related protein 3 (LHCSR3) is crucial for the qE mechanism. LHCSR3 expression is observed in various conditions that result in photooxidation, such as exposure to high light or nutrient deprivation, where the amount of captured light surpasses the maximum photosynthetic capacity. Although the role of LHCSR3 has been extensively studied under high light (HL) conditions, its function during nutrient starvation remains unclear. In this study, we demonstrate that LHCSR3 expression can occur under light intensities below saturation without triggering qE, particularly when nutrients are limited. To investigate this, we cultivated C. reinhardtii cells under osmotic stress, which replicates conditions of nutrient scarcity. Furthermore, we examined the photosynthetic membrane complexes of wild-type (WT) and npq4 mutant strains grown under osmotic stress. Our analysis revealed that LHCSR3 expression might modify the interaction between the photosystem II core and its peripheral light-harvesting complex II antennae. This alteration could potentially impede the transfer of excitation energy from the antenna to the reaction center. •The LHCSR3 expression is induced in osmotic stress, and its photoprotective function does not involve qE.•Photosystem II core D1 is protected by LHCSR3 expression.•The LHCSR3 expression affects the interaction between the PSII core with its peripheral LHCII antenna.•Thylakoid lumen acidification is essential for the expression and function of LHCSR3.•However, the expression of LHCSR3 induced changes in photosynthetic efficiency.