Lempiäinen Tapio, Muth-Pawlak Dorota, Vainonen Julia P, Rintamäki Eevi, Tikkanen Mikko, Aro Eva-Mari
Molecular Plant Biology, Department of Life Technologies, University of Turku, Turku, Finland.
Physiol Plant. 2025 May-Jun;177(3):e70298. doi: 10.1111/ppl.70298.
In nature, environmental conditions are constantly changing, requiring plants to have numerous regulatory mechanisms to keep light harvesting and metabolism in balance. Here, we show that high light (HL) induces a much stronger non-photochemical quenching (NPQ) when lettuce plants are exposed to 1500 μmol photons m s for 4 h at 13°C (low temperature, LT) compared to 23°C (growth temperature, GT). GT/HL treatment induced NPQ to relax during 1 h in darkness. In contrast, LT/HL treatment induced an exceptionally high NPQ that only partially relaxed during 1 h in darkness at GT. Such a high sustained NPQ (sNPQ) cannot be explained by the canonical NPQ mechanism(s). Instead, sNPQ was associated with a transient increase in phosphorylation of minor LHCII antenna proteins, LHCB4.1/LHCB4.2 and partial disassembly of PSII-LHCII complexes. This coincided with increased expression of the light-harvesting-like proteins SEP2 and ELIP1.2, the PSII assembly proteins HCF173 and LPA3, and accumulation of the pre-D1 protein, indicating delayed PSII repair. These results lead us to propose that under LT/HL, the phosphorylation of LHCB4.1/LHCB4.2 initiates the disassembly of PSII-LHCII supercomplexes, allowing accumulated SEP2 to bind to CP47, presumably leading to quenching of the inner PSII core antenna. The free CP43 core antenna, released from PSII at an early stage of repair, is proposed to be protected by accumulated LPA3. Apparently, the cascades of regulatory mechanisms are specific to each combination of environmental changes, depending on their concomitant effects on chloroplast redox balance and PSII repair rate, with induced PSII core antenna quenching contributing to sNPQ.
在自然界中，环境条件不断变化，这就要求植物具备众多调节机制，以维持光捕获与新陈代谢的平衡。在此，我们发现，与在23°C（生长温度，GT）相比，当生菜植株在13°C（低温，LT）下暴露于1500 μmol光子·m⁻²·s⁻¹ 4小时（高光，HL）时，高光诱导出更强的非光化学猝灭（NPQ）。GT/HL处理诱导的NPQ在黑暗中1小时内松弛。相比之下，LT/HL处理诱导出异常高的NPQ，在GT下黑暗中1小时内仅部分松弛。这种高持续NPQ（sNPQ）无法用典型的NPQ机制来解释。相反，sNPQ与次要LHCII天线蛋白LHCB4.1/LHCB4.2磷酸化的短暂增加以及PSII-LHCII复合物的部分解体有关。这与类光捕获蛋白SEP2和ELIP1.2、PSII组装蛋白HCF173和LPA3的表达增加以及前体D1蛋白的积累同时发生，表明PSII修复延迟。这些结果使我们提出，在LT/HL条件下，LHCB4.1/LHCB4.2的磷酸化引发PSII-LHCII超复合物的解体，使积累的SEP2能够与CP47结合，大概导致PSII内部核心天线的猝灭。从PSII修复早期释放的游离CP43核心天线，被认为由积累的LPA3保护。显然，调节机制的级联对于环境变化的每种组合都是特定的，这取决于它们对叶绿体氧化还原平衡和PSII修复速率的伴随影响，诱导的PSII核心天线猝灭导致了sNPQ。
