Heat Stress

Heat is understood here as the upper temperature range in which active life is possible (Fig. 4.1). In this range, stress increases with increasing temperature, and organisms (in particular, plants) that cannot escape the heat stress respond with a diverse set of reactions. Not all of them are specific to heat; they can also be observed under drought, salt and heavy metal strain—that is, whenever proteins are denatured. Nevertheless the heat stress response in plants has distinctive features and is very complex. In the tolerable temperature range it appears to follow the stress dose rule (the product of the severity of stress and exposure time: ∆Т x t) (Nover and Hohfeld 1996).

In mesophilic plants a slight heat stress response can be observed beyond 35 °C. Above 40 °C, strong reactions take place. Such temperatures can be reached in many plant habitats. On a sunny day in Central Europe, for instance, topsoil temperatures can transitorily exceed 50 °C, which can severely damage or even kill seedlings that have just emerged from the soil surface. Also, solar irradiation can cause very rapid increases in temperature by easily 20 °C within minutes (McClung and Davis 2010).

Heat damage (Fig. 4.26) is predominantly a consequence of protein misfolding and protein denaturation (Fig. 4.2). Additionally, the functionality of membranes is negatively affected by excessive fluidity. Molecular interactions between membrane components are weakened, which can cause ion leakage. Some processes, including photosynthesis, are more sensitive to heat than others. Among the developmental stages of plants, seedling development and reproduction are particularly vulnerable (Bita and Gerats 2013).

Fig. 4.26. Heat damage on a leaf of Cannabis sativa, resulting in collapsed leaf patches. The pale colour indicates disintegration of the chloroplasts and photobleaching of chlorophyll liberated from their protein environment in the thylakoids. (Source: http://forum.sensiseeds.com/ images/plant_problems/heat_stress_rd_c2727.html)

When one is considering the exposure of a plant to potentially dangerous elevated temperatures, heat shock should be differentiated from heat stress. A heat shock (even if it is not injurious) refers to a sudden and short-term exposure that triggers a transient short-term response, while heat stress refers to a long-term exposure to elevated and potentially damaging temperatures. Both heat shock and heat stress can lead to the so-called acquired thermotolerance - that is, the ability to withstand higher temperatures because of acclimation.

The major difference at the cellular level is the rapid deceleration of housekeeping metabolism (apparent in the down-regulation of housekeeping genes) and the subsequent revival of this metabolism after a return to the normal temperature in the heat shock reaction, while in long-term heat stress exposure the housekeeping metabolism has to maintain its function at the elevated temperature. Both sets of reactions, however, depend on the strongly enhanced expression of genes encoding transcription factors (heat shock factors) and protective proteins (heat shock proteins), many of which serve essential cellular functions also at optimal temperature.

Even in the absence of actual heat stress, temperature optima of plants differ both between and within species. Temperatures beyond the optimal range not only accelerate but also redirect metabolic processes and lead to changes in metabolite pools, thereby affecting growth and many other developmental processes. A good example of differential responses to elevated temperatures below the heat stress threshold is provided by potatoes (Solanum tuberosum; Table 4.10) (Lafta and Lorenzen 1995), which originate from the tropical Andes. Despite being cultivated for ~13,000 years, potatoes still have a rather narrow range of optimal growth temperatures. As tropical upland plants, potatoes grow best at temperatures around 20 °C. More than 5000 potato cultivars are currently known, some of which are considered heat tolerant (e.g. cv. “Norchip”), while others are heat sensitive (e.g. cv. “Up-to-date”).

Table 4.10. Effects of elevated temperatures on growth, tuber formation and starch content of a heat-tolerant potato (Solanum tuberosum) variety (“Norchip”) and a heat-sensitive variety (“Up-to-date”) (Lafta and Lorenzen 1995). Control plants were grown under a day/night temperature regime of 19/17 °C; plants exposed to elevated temperatures grew at 31/29 °C. Biomass production and growth of the potato plants were determined after 4 weeks of heat stress, which started at the onset of tuber formation. The starch content of fully developed leaves was measured 8 days after the temperature increase at the end of the daily light period

Growth at elevated temperature results in a change in the developmental control system of both cultivars, as shown in Table 4.10. “Norchip” was less affected than “Up-to date” but tuber formation was strongly suppressed in both varieties along with a drastically reduced starch formation and storage. Instead, elongation growth of the shoots was increased.

Starch formation in the tubers (“sink”) requires phloem unloading by sucrose synthase and formation of the starch synthase substrate adenosine diphosphate (ADP)-glucose by ADP-glucose pyrophosphorylase. Both enzyme activities were significantly decreased by heat stress (Table 4.11). In contrast, sucrose metabolism was slightly increased or at least not attenuated.

Table 4.11. Activities of the enzymes starch synthase and ADP-glucose pyrophosphorylase (AGPase) in the potato tubers of “Norchip” and “Up-to-date” after 2 weeks of exposure to an elevated temperature regime (from Lafta and Lorenzen (1995)

Fig. 4.27. Effects of heat on plants and their reactions to it

Such effects of temperatures below the threshold of heat stress will not be discussed further here. The main focus of this chapter is the variety of cellular mechanisms of heat survival, which are summarised in Fig. 4.27.