Non-photochemical quenching (NPQ) helps dissipate surplus light energy, preventing formation of reactive oxygen species (ROS). In Chlamydomonas reinhardtii, the thylakoid membrane protein LHCSR3 is involved in pH-dependent (qE-type) NPQ, lacking in the npq4 mutant. Preventing PSII repair revealed that npq4 lost PSII activity faster than the wild type (WT) in elevated O2, while no difference between strains was observed in O2-depleted conditions. Low Fv/Fm values remained 1.5 h after moving cells out of high light, and this qH-type quenching was independent of LHCSR3 and not accompanied by losses of maximum PSII activity. Culturing cells in historic O2 atmospheres (30-35%) increased the qE of cells, due to increased LHCSR1 and PsbS levels, and LHCSR3 in the WT, showing that atmospheric O2 tensions regulate qE capacity. Colony growth of npq4 was severely restricted at elevated O2, and npq4 accumulated more reactive electrophile species (RES) than the WT, which could damage PSI. Levels of PsaA (PSI) were lower in npq4 grown at 35% O2, while PsbA (PSII) levels remained stable. We conclude that even at high O2 concentrations, the PSII repair cycle is sufficient to maintain net levels of PSII. However, LHCSR3 has an important function in protecting PSI against O2-mediated damage, such as via RES.

中文翻译：

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非光化学淬灭蛋白LHCSR3可防止莱茵衣藻中氧依赖性光抑制作用。

非光化学淬灭（NPQ）有助于消散多余的光能，防止形成活性氧（ROS）。在莱茵衣藻中，类囊体膜蛋白LHCSR3参与pH依赖性（qE型）NPQ，而npq4突变体则缺乏。预防PSII修复显示，在升高的O2中，npq4失去PSII活性的速度比野生型（WT）快，而在O2耗尽的条件下，菌株之间没有差异。将细胞移出高光后1.5 h，仍保持低Fv / Fm值，并且该qH型猝灭独立于LHCSR3，并且不会伴随最大PSII活性的丧失。在历史性的O2大气中培养细胞（30-35％），这是由于LHCSR1和PsbS水平以及WT中的LHCSR3增加，从而提高了细胞的qE，这表明大气中的O2张力调节了qE容量。在升高的O2浓度下，npq4的菌落生长受到严格限制，并且npq4积累的反应性亲电物质（RES）比WT多，这可能会破坏PSI。在35％O2下生长的npq4中，PsaA（PSI）的水平较低，而PsbA（PSII）的水平保持稳定。我们得出结论，即使在高O2浓度下，PSII修复周期也足以维持PSII的净水平。但是，LHCSR3在保护PSI免受O2介导的损害（例如通过RES）方面具有重要功能。