Abstract
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.
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