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Quantifying the long-term interplay between photoprotection and repair mechanisms sustaining photosystem II activity
Biochemical Journal ( IF 4.1 ) Pub Date : 2022-03-18 , DOI: 10.1042/bcj20220031
Francesco Saccon 1 , Sam Wilson 1 , Felix S. Morey-Burrows 2 , ALEXANDER V. RUBAN 1
Affiliation  

The photosystem II reaction centre (RCII) protein subunit D1 is the main target of light-induced damage in the thylakoid membrane. As such, it is constantly replaced with newly synthesised proteins, in a process dubbed the ‘D1 repair cycle’. The mechanism of relief of excitation energy pressure on RCII, non-photochemical quenching (NPQ), is activated to prevent damage. The contribution of the D1 repair cycle and NPQ in preserving the photochemical efficiency of RCII is currently unclear. In this work, we seek to (1) quantify the relative long-term effectiveness of photoprotection offered by NPQ and the D1 repair cycle, and (2) determine the fraction of sustained decrease in RCII activity that is due to long-term protective processes. We found that while under short-term, sunfleck-mimicking illumination, NPQ is substantially more effective in preserving RCII activity than the D1 repair cycle (Plant. Cell Environ.41, 1098–1112, 2018). Under prolonged constant illumination, its contribution is less pronounced, accounting only for up to 30% of RCII protection, while D1 repair assumes a predominant role. Exposure to a wide range of light intensities yields comparable results, highlighting the crucial role of a constant and rapid D1 turnover for the maintenance of RCII efficiency. The interplay between NPQ and D1 repair cycle is crucial to grant complete phototolerance to plants under low and moderate light intensities, and limit damage to photosystem II under high light. Additionally, we disentangled and quantified the contribution of a slowly reversible NPQ component that does not impair RCII activity, and is therefore protective.

中文翻译:

量化维持光系统 II 活性的光保护和修复机制之间的长期相互作用

光系统 II 反应中心 (RCII) 蛋白亚基 D1 是类囊体膜中光诱导损伤的主要目标。因此,在被称为“D1 修复周期”的过程中,它不断被新合成的蛋白质取代。RCII 上的激发能量压力释放机制,即非光化学猝灭 (NPQ),被激活以防止损坏。目前尚不清楚 D1 修复周期和 NPQ 在保持 RCII 光化学效率方面的贡献。在这项工作中,我们寻求 (1) 量化 NPQ 和 D1 修复周期提供的光保护的相对长期有效性,以及 (2) 确定由于长期保护过程导致的 RCII 活性持续下降的比例. 我们发现,在短期的、模仿太阳斑点的光照下,NPQ 在保持 RCII 活性方面​​比 D1 修复周期更有效(Plant. Cell Environ.41, 1098–1112, 2018)。在长时间的恒定光照下,其贡献不那么明显,仅占 RCII 保护的 30%,而 D1 修复则占主导地位。暴露在广泛的光强度下会产生可比较的结果,突出了持续快速的 D1 周转对维持 RCII 效率的关键作用。NPQ 和 D1 修复周期之间的相互作用对于在低和中等光强度下赋予植物完全的光耐受性以及限制强光下对光系统 II 的损害至关重要。此外,我们解开并量化了不损害 RCII 活性的缓慢可逆 NPQ 成分的贡献,因此具有保护作用。
更新日期:2022-03-16
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