Exposure of Arabidopsis (Arabidopsis thaliana) to 4°C imprints a cold memory that modulates gene expression in response to a second (triggering) stress stimulus applied several days later. Comparison of plastid transcriptomes of cold-primed and control plants directly before they were exposed to the triggering stimulus showed downregulation of several subunits of chloroplast NADPH dehydrogenase (NDH) and regulatory subunits of ATP synthase. NDH is, like proton gradient 5 (PGR5)–PGR5-like1 (PGRL1), a thylakoid-embedded, ferredoxin-dependent plastoquinone reductase that protects photosystem I and stabilizes ATP synthesis by cyclic electron transport (CET). Like PGRL1A and PGRL1B transcript levels, ndhA and ndhD transcript levels decreased during the 24-h long priming cold treatment. PGRL1 transcript levels were quickly reset in the postcold phase, but expression of ndhA remained low. The transcript abundances of other ndh genes decreased within the next days. Comparison of thylakoid-bound ascorbate peroxidase (tAPX)-free and transiently tAPX-overexpressing or tAPX-downregulating Arabidopsis lines demonstrated that ndh expression is suppressed by postcold induction of tAPX. Four days after cold priming, when tAPX protein accumulation was maximal, NDH activity was almost fully lost. Lack of the NdhH-folding chaperonin Crr27 (Cpn60β4), but not lack of the NDH activity modulating subunits NdhM, NdhO, or photosynthetic NDH subcomplex B2 (PnsB2), strengthened priming regulation of zinc finger of A. thaliana 10, which is a nuclear-localized target gene of the tAPX-dependent cold-priming pathway. We conclude that cold-priming modifies chloroplast-to-nucleus stress signaling by tAPX-mediated suppression of NDH-dependent CET and that plastid-encoded NdhH, which controls subcomplex A assembly, is of special importance for memory stabilization.

中文翻译：

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抗坏血酸过氧化物酶冷后调节叶绿体 NADPH 脱氢酶活性控制冷记忆

将拟南芥 (Arabidopsis thaliana) 暴露在 4°C 下会留下冷记忆，该记忆会调节基因表达，以响应几天后施加的第二次（触发）应激刺激。在暴露于触发刺激之前，对冷启动植物和对照植物的质体转录组进行比较，结果显示叶绿体 NADPH 脱氢酶 (NDH) 的几个亚基和 ATP 合酶的调节亚基下调。NDH 与质子梯度 5 (PGR5)–PGR5-like1 (PGRL1) 一样，是一种类囊体嵌入的铁氧还蛋白依赖性质体醌还原酶，可保护光系统 I 并通过循环电子传递 (CET) 稳定 ATP 合成。与 PGRL1A 和 PGRL1B 转录水平一样，ndhA 和 ndhD 转录水平在 24 小时长引发冷处理期间下降。PGRL1 转录水平在冷后阶段迅速重置，但 ndhA 的表达仍然较低。其他 ndh 基因的转录本丰度在接下来的几天内下降。类囊体结合的抗坏血酸过氧化物酶 (tAPX) 无和瞬时 tAPX 过表达或 tAPX 下调拟南芥品系的比较表明，ndh 表达受到 tAPX 冷后诱导的抑制。冷引发后四天，当 tAPX 蛋白积累达到最大时，NDH 活性几乎完全丧失。缺乏 NdhH 折叠伴侣蛋白 Crr27 (Cpn60β4)，但不缺乏 NDH 活性调节亚基 NdhM、NdhO 或光合 NDH 亚复合体 B2 (PnsB2)，加强了拟南芥 10 锌指的启动调节，拟南芥 10 是核拟南芥的锌指。 -tAPX依赖性冷启动途径的定位靶基因。我们得出的结论是，冷启动通过 tAPX 介导的 NDH 依赖性 CET 抑制来改变叶绿体到细胞核的应激信号传导，并且质体编码的 NdhH（控制亚复合物 A 组装）对于记忆稳定特别重要。