Abstract：
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.
摘要：
植物有一种称为非光化学猝灭的保护机制，以防止阳光过多造成的损害。该机制的关键组成部分是能量依赖性猝灭(qE)。在莱茵衣藻中，这种称为捕光复合应激相关蛋白3（LHCSR3）的蛋白表达对于qE机制至关重要。在导致光氧化的各种条件下观察到LHCSR3表达，例如暴露于强光或营养匮乏，捕获的光量超过最大光合能力。尽管LHCSR3在强光(HL)条件下的作用已得到广泛研究，其在营养饥饿期间的功能仍不清楚。在这项研究中,我们证明LHCSR3表达可以在低于饱和的光强度下发生，而不会触发QE，特别是当营养有限时。为了调查这一点，我们在渗透胁迫下培养了莱茵酵母细胞，这复制了营养匮乏的条件。此外，我们检查了在渗透胁迫下生长的野生型（WT）和npq4突变株的光合膜复合物。我们的分析表明，LHCSR3的表达可能会改变光系统II核心与其外围捕光复合物II触角之间的相互作用。这种改变可能潜在地阻碍激发能量从天线到反应中心的传递。
