When it suddenly gets extremely hot in summer – or when a growth chamber accidentally overheats – plants get stressed. As heat can cause permanent damage and is sometimes even lethal, plants have several mechanisms to protect themselves. They have a certain basal ability to survive temperatures above the optimum for growth, and when extreme directly preceded by a period of mild heat, they can survive better by acquiring thermotolerance (Yeh et al., 2012). In nature, however, high temperatures often occur repeatedly. To cope with this, plants have evolved an intricate mechanism: after experiencing heat once, they can deal better with high temperatures when the heat recurs (Bäurle, 2016). The idea that plants might be able to remember stressful events to cope better with similar situations later has been around for a while (e.g. Itai and Benzioni, 1976). However, evidence for it did not start to accumulate until the mid‐2000s. The idea was rather enigmatic. Plants, non‐cognitive organisms without a nervous system, were somehow able to construct a memory of past events. In search of the underlying mechanisms, the focus quickly turned towards the role of chromatin (Chinnusamy and Zhu, 2009). Epigenetic alterations such as histone modifications and DNA methylation can alter gene expression patterns, which can then be stably propagated. This might be convenient for acquiring a molecular memory. Indeed, epigenetic regulation turned out to play a key role in a range of different stress memories, such as for drought, salinity, cold and heat (Kim et al., 2015). The research towards heat‐stress memory is fueled by imminent climate change, with more frequent and intense heatwaves. Isabel Bäurle in Potsdam, Germany, is one of the scientists investigating the underlying pathways. Her group is especially interested in the role of epigenetic and chromatin regulation in the adaptation of plants to stress. For example, in the last several years they have uncovered the role of FORGETTER 1 (FGT1), a protein that interacts with chromatin remodelers of the SWI/SNF and ISWI families, that mediates heat‐stress memory by modulating nucleosome occupancy (Brzezinka et al., 2016). In this issue of The Plant Journal, her team identified two genes that are crucial for heat‐stress memory. Surprisingly, these genes encode a protein phosphatase and a phospholipase, and are not directly involved in epigenetic regulation.

The protein phosphatase was identified in a mutagenesis screen and designated as FORGETTER 2 (FGT2). When the authors performed heat‐stress experiments with the mutant plants, they observed that they were specifically defective in heat‐stress memory, but not in the initial acquisitison of thermotolerance (Figure). Protein phosphatases are enzymes that remove phosphate groups from proteins. By altering the phosphorylation status, they control whether a protein is active or not. The class of type‐2C protein phosphatases to which FGT2 belongs is known to play prominent roles in plant stress responses (Singh et al., 2015). Until now, however, they have never been implicated in heat‐stress memory.

When the authors isolated interaction partners of FGT2 they found phospholipase Dα2 (PLDα2). Mutant analyses confirmed that the gene encoding this enzyme was also critical for heat‐stress memory. Moreover, the fgt2 pldα2 double mutant reacted in the same way to heat stress as the fgt2 single mutant, suggesting that the two genes act in the same genetic pathway. Phospholipases of the D class hydrolyze phospholipids and release phosphatidic acid. As biological membranes are mainly made up of phospholipids, the action of phospholipases plays an important role in their stability and structure. Furthermore, both phospholipids and phosphatidic acid are known to function as signaling molecules. Bäurle and her team showed that PLDα2 resided in the cytoplasm, whereas FGT2 attaches to the plasma membrane, probably through lipid anchoring. They suggest a model in which FGT2 and PLDα2 interact at the plasma membrane–cytosol interface. FGT2 might be responsible for the dephosphorylation of PLDα2, thereby controlling its activity (Figure 1). The phospholipase activity of PLDα2 might alter the lipid composition of the cell membrane or produce signaling molecules that induce heat‐stress memory. The exact downstream pathway that eventually leads to this ‘memory’ of heat stress remains enigmatic. It is possible that chromatin remodeling is taking place further downstream, but it might as well be an independent mechanism.

As Bäurle’s team is particularly focused on the role of epigenetic regulation in plant stress, discovering that FGT2 and PLDα2 are involved is remarkable. Bäurle calls it the beauty of forward genetics; it can yield new and unexpected findings that do not fit in your model (yet). It also underlines the importance of using unbiased approaches. She hopes that their new findings will inspire the work of others studying stress responses, protein phosphatases, phospholipases, membrane dynamics and stress memory, in foreseeable and unforeseeable ways. All good reasons to heat up your growth chambers.

当夏季突然变得极热时–或生长室意外过热时–植物就会感到压力。由于热量会造成永久性损害，有时甚至是致命的，植物具有多种保护自身的机制。它们具有一定的基本能力，可以在高于最佳生长温度的温度下生存，并且在极端情况下直接经过一段温和的高温后，可以通过获得耐热性来更好地生存（Yeh等人，2012）。但是，实际上，高温经常反复发生。为了解决这个问题，植物进化出了一种复杂的机制：经历一次热后，当热量再次出现时，它们可以更好地应对高温（Bäurle，2016）。植物可能能够记住压力事件以更好地应对类似情况的想法已经存在了一段时间（例如Itai和Benzioni，1976）。但是，直到2000年代中期才开始积累证据。这个想法很神秘。植物是没有神经系统的非认知生物，能够以某种方式构建对过去事件的记忆。在寻找潜在的机制时，焦点迅速转向了染色质的作用（Chinnusamy和Zhu，2009年）。）。表观遗传学改变（例如组蛋白修饰和DNA甲基化）可以改变基因表达模式，然后可以稳定地繁殖。这对于获取分子记忆可能很方便。确实，表观遗传调控在一系列不同的应力记忆中起着关键作用，例如在干旱，盐分，寒冷和高温下（Kim等，2015）。）。迫在眉睫的气候变化推动了热应激记忆的研究，热浪更加频繁和强烈。位于德国波茨坦的IsabelBäurle是研究潜在途径的科学家之一。她的小组对表观遗传和染色质调节在植物适应胁迫中的作用特别感兴趣。例如，在最近几年中，他们发现了FORGETTER 1（FGT1）的作用，该蛋白与SWI / SNF和ISWI家族的染色质重塑剂相互作用，通过调节核小体的占用来介导热应激记忆（Brzezinka等。，2016）。在本期《植物杂志》中，她的团队确定了两个对热应激记忆至关重要的基因。令人惊讶的是，这些基因编码蛋白质磷酸酶和磷脂酶，并且不直接参与表观遗传调控。

在诱变筛选中鉴定出蛋白质磷酸酶，并将其命名为FORGETTER 2（FGT2）。当作者对突变植物进行热胁迫实验时，他们观察到它们在热胁迫记忆中特别有缺陷，但在最初的耐热性习性中没有缺陷（图）。蛋白质磷酸酶是从蛋白质中除去磷酸基团的酶。通过改变磷酸化状态，它们可以控制蛋白质是否具有活性。已知FGT2所属的2C型蛋白质磷酸酶在植物胁迫反应中起着重要作用（Singh等，2015）。但是，到目前为止，它们从未涉及热应激记忆。

当作者分离FGT2的相互作用伴侣时，他们发现了磷脂酶Dα2（PLDα2）。突变分析证实，编码该酶的基因对于热应激记忆也很关键。此外，fgt2pldα2双重突变体以与fgt2相同的方式对热应激反应单个突变体，表明这两个基因在同一遗传途径中起作用。D类的磷脂酶水解磷脂并释放出磷脂酸。由于生物膜主要由磷脂组成，因此磷脂酶的作用对其稳定性和结构起重要作用。此外，已知磷脂和磷脂酸都起信号分子的作用。Bäurle和她的研究小组表明PLDα2驻留在细胞质中，而FGT2可能通过脂质锚定附着在质膜上。他们提出了一个模型，其中FGT2和PLDα2在质膜-细胞溶胶界面相互作用。FGT2可能负责PLDα2的去磷酸化，从而控制其活性（图1）。PLDα2的磷脂酶活性可能会改变细胞膜的脂质组成或产生诱导热应激记忆的信号分子。最终导致这种热应激“记忆”的确切下游途径仍然是个谜。染色质重塑可能发生在更下游，但也可能是独立的机制。

由于Bäurle的团队特别关注表观遗传调控在植物胁迫中的作用，因此发现FGT2和PLDα2参与其中非常重要。Bäurle称其为前向遗传学之美。它会产生新的和出乎意料的发现，这些发现并不适合您的模型（尚未）。它还强调了使用无偏见方法的重要性。她希望他们的新发现会启发其他人以可预见和不可预见的方式研究应激反应，蛋白质磷酸酶，磷脂酶，膜动力学和应激记忆的工作。所有充分的理由加热您的生长室。