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Perception of Stress and Creation of Signals

How is stress, as a multifactorial complex, detected and how is the signal triggering the stress reaction produced? It is known that pathogens produce degradation products of their own cell walls or of the cell walls of the host plant, termed elicitors, which trigger a response, mostly synthesis of so-called phytoalexins (see Chaps. 1.3.5.1 and 1.10.2). But how does abiotic stress - cold, heat, mechanical stress, osmotic stress, lack of oxygen - become a signal? How specific are such signals? Can hardening occur even without stress?

Little is known about the perception of abiotic stress at the molecular level. An example is the perception of osmotic stress in the unicellular green alga Dunaliella salina. This alga does not produce a firm cell wall but it is able to adapt its osmotic potential to that of the medium (0.1-5.5 M NaCl in the medium) and so avoids dramatic changes in volume. Adaptation to the osmotic potential of the medium is accomplished exclusively through the metabolite glycerol, one of the compatible solutes which in a medium saturated with NaCl accumulates up to 60% of the cell weight. Upon hyperosmotic shock the cell shrinks transiently, but is able to regain its original volume within 30-120 min through glycerol production. The mechanism by which glycerol accumulates in cells without leaching into the medium is not known. De novo synthesis of new proteins is apparently not involved. Furthermore, stressor specificity is

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| Fig. 1.1.8. The stress concept according to Beck and Luttge. A Relationship between stress and strain in a system that is not capable of hardening (e.g. chilling of the African violet, cf. Fig. 1.1.6). The stress factor time is not considered. B Relationship between strain and duration of stress in a system capable of repair and hardening. C Relationship of strain and stress allowing also for time as a factor that increases or alleviates stress. The system under consideration is capable of hardening (e.g. frost hardening of spruce needles in autumn). For clarification, two panels are inserted into the three-dimensional coordinate system in the transition zone between elastic and plastic strain. (After Beck and Luttge 1990)

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Normal condition low, as other osmotica, e.g. polyols, if producing hyperosmotic stress, likewise trigger glycerol accumulation. It is assumed that the transient shrinking process itself produces the signal (see Fig, 1.3.18). Consequently, there are two possibilities for the creation of signals: a sensor located in the plasma membrane (see Chap. 1.2.2.1) or, arising from the contraction of volume, exceeding a threshold concentration of a metabolite in the cytosol. There is more support for the first possibility. A transient, short-term stiffening of the membrane appears to be important, which results in a closer packing of the lipid molecules in the bilayer (a volume contraction must, after all, also lead to a decrease in the surface of the plasma membrane, see Fig. 1.3.18). The high sterol content of the plasma membrane appears to be important in this respect for signal creation (sterols form 35-45% of the total lipids of the cell!). If cells are stressed in the presence of an inhibitor of steroid biosynthesis ("tride-morph"), the sterol content of the membrane is dramatically decreased. At the same time, the ability of the cell to regain its volume by glycerol accumulation after a hyperosmotic shock is lost. The effect of the inhibitor can be completely reversed if an artificial sterol (cholesterol hemisuc-cinate) is applied to the cells via the medium. It is assumed in the model shown in Fig, 1.1.9 that sterols interact in such a way with an osmosen-sor protein located in the membrane that the protein is activated by membrane stiffening. Perception of cold is probably also via cold-triggered stiffening of the membrane (Sung et al. 2003).

With respect to regularly recurring stresses, as for example frost in winter, "feed-forward" signals could be suggested, which might trigger the hardening process without the perception of a stress. It has been shown that shortening of day length induces frost hardening in pine. Temperatures around freezing point are also effective (even under a long-day light period). In the end, both signals lead to the same frost hardening, but the process induced by short days takes considerably longer (0.4°C/day) than that triggered by cold (0.9 °C/day; Hansen and Beck 2002). A transient increase in viscosity of biomembranes appears to act as a cellular signal as in Dunaliella (see also Vigh et al. 1993). In nature, both factors perform synergetically, but the decreasing day length in autumn is probably always the first triggering signal. It has been proven that the phytochrome and cryptochrome systems both take part in the triggering of frost hardening (and dehardening). However, little is known about signal transduction in the cell (cf. Chap. 1.3.6.1).

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Sensor in activated condition

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