At dawn of a scorching summer day, land plants must anticipate upcoming extreme midday temperatures by timely establishing molecular defences that can keep heat-labile membranes and proteins functional. A gradual morning pre-exposure to increasing sub-damaging temperatures induces heat-shock proteins (HSPs) that are central to the onset of plant acquired thermotolerance (AT). To gain knowledge on the mechanisms of AT in the model land plant Physcomitrium patens, we used label-free LC–MS/MS proteomics to quantify the accumulated and depleted proteins before and following a mild heat-priming treatment. High protein crowding is thought to promote protein aggregation, whereas molecular chaperones prevent and actively revert aggregation. Yet, we found that heat priming (HP) did not accumulate HSP chaperones in chloroplasts, although protein crowding was six times higher than in the cytosol. In contrast, several HSP20s strongly accumulated in the cytosol, yet contributing merely 4% of the net mass increase of heat-accumulated proteins. This is in poor concordance with their presumed role at preventing the aggregation of heat-labile proteins. The data suggests that under mild HP unlikely to affect protein stability. Accumulating HSP20s leading to AT, regulate the activity of rare and specific signalling proteins, thereby preventing cell death under noxious heat stress.

中文翻译：

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定量蛋白质组学分析以捕捉热积累蛋白质在苔藓植物获得的耐热性中的作用

在炎热的夏日黎明时分，陆地植物必须通过及时建立分子防御来保持不耐热的膜和蛋白质的功能，从而预测即将到来的极端中午温度。早上逐渐暴露于增加的亚损伤温度会诱导热休克蛋白 (HSP)，这是植物获得性耐热性 (AT) 发作的核心。了解模式陆生植物Physcomitrium patens中 AT 的机制，我们使用无标记 LC-MS/MS 蛋白质组学来量化在温和热引发处理之前和之后积累和消耗的蛋白质。高蛋白质拥挤被认为促进蛋白质聚集，而分子伴侣阻止并积极地恢复聚集。然而，我们发现热启动 (HP) 不会在叶绿体中积累 HSP 分子伴侣，尽管蛋白质拥挤程度是细胞质中的六倍。相比之下，几个 HSP20 在细胞质中强烈积累，但仅占热积累蛋白质净质量增加的 4%。这与它们在防止热不稳定蛋白质聚集方面的假定作用不一致。数据表明，在轻度 HP 下不太可能影响蛋白质稳定性。积累导致 AT 的 HSP20，