1 .4.1 . Metabolism at High Temperature
The ability of biological entities to grow at high temperature has been known for almost 200 years, with a considerable body of the literature being . concerned with thermal stability. Many of these studies have addressed the question of how organisms live at high temperatures which would normally
destroy or inactivate the cellular components of most forms of life. Two explanations have been offered : the first (and most obvious) is that the essential cell components of thermophilic forms are relatively more heat stable than those of their mesophyllic counterparts, the second is that the cells are capable of rapid resynthesis of the destroyed or inactivated components ( Campbe/1 and Pace 1 968).
From a physiological viewpoint, a decrease in photosynthesis and an increase in the degradation of protein and carbohydrates will lead to a decrease in dry
m atter accumulation. The work of Al-khatib and Paulsen {1 984) showed that
high temperatures accelerated the normal decline in viable leaf blade area and photosynthetic activities per unit area, electron transport declined earlier and faster than other photosynthetic processes at the suitable temperature, and protease activity during senescence was markedly accentuated. They suggested that a major effect of high temperature was the acceleration of the deterioration of photosynthetic activities, and the degradation of proteinaceous constituents.
1t has been suggested that the primary effect of high temperature is the dis�uption of cell metabolism, possibly by protein denaturation, or by the
production of toxic substances or by membrane damage ( Fitter and Hay
1 98 1 ). Some toxins produced in heated leaves, can be translocated and then
injure the unheated leaves ( Yarwood 1 961 ).
C3 plants (such as asparagus; Downton and Torokfalvy 1 975) exhibit a decline
in photosynthetic rate at high temperatures. There is a large scope for m odification of the temperature effects via modification of RuDP carboxylase
properties (Ehleringer and Bjorkman 1 977; Berry and Bjorkman 1 980). As
temperatures increase, the specific enzymatic activities of the photosynthetic apparatus are lost and specific function of the photosynthetic membranes are
altered (Berry and Bjorkman). Thus the changes in the thylakoid membrane
Heat inactivation of biomembranes may be prevented by the synthesis or accumulation of protective compounds such as heat shock proteins surrounding the membrane or by biochemical and /or ultrastructural changes
within the membrane (Santarius 1 973; Krause and Santarius 1 975; Thebud
and Santarius 1 982}. However in connection with the stabilizing effect of
soluble non-sugar stroma compounds, Santarius and MOl/er {1 979} proposed
that changes in the ultrastructure of thylakoids are responsible for acclimation of the photosynthetic apparatus to high temperature conditions.
Gent and Enoch {1 983) citing previous work showed that at a constant
temperature plant growth rate was linearly related to the photosynthetic rate, but the effect of temperature on growth and photosynthesis was not the same, because the photosynthetic rate increased with temperature in an asymptotic manner to a plateau above 1 5°C, but the growth rate increased exponentially
from 5°C to 20°C and fell rapidly at temperatures above 25°C. The divergence
occurred because only a part of the assimilates was used to promote growth and the rest is used to maintain the plant in the current state, that is respiration could be divided into maintenance respiration and growth respiration (Thomley 1 977; Barnes and Hole 1 978). Although growth respiration and maintenance
respiration increased exponentially up to 20°C, maintenance respiration was
promoted by higher temperature, while growth respiration was not (McCree 1 97 4). Therefore, thermoperiodism (warm days and cool nights) may result in
faster growth than constant temperature due to the high levels of nonstructural carbohydrate used for growth and smaller requirement for maintenance during cool nights (Szaniawski 1 983). At high temperature growth is limited by the
supply of nonstructural carbohydrate due to maintenance having priority for no� structural carbohydrate. The optimal temperature for growth maintains both a high rate of supply of carbohydrate and energy to convert to structural material (Gent and Enoch 1 983}. However often growth is at least as fast at
constant temperatures (Robson 1 972, 1 973; Warrington et al 1 977; McCree
. and Amthor 1 982},-perhaps because low night temperatures may lead to a
Blackman ( 1 975) concluded that a difference between the night and day
temperature has been found to have a positive effect only when a sub-optimal day temperature is combined with a supra-optimal night temperature.
Gerik and Eastin (1 985) with sorghum showed that growth respiration is less .
dependent on temperature, and maintenance respiration is strongly dependent on temperature. In fact, maintenance respiration is not only strongly modified by temperature, but also depends on growth rate, and varies with plant organs
(e.g. root > top) (McCree 1 974; Hansen and Jensen 1 9n; McCree and
Silsbury 1 978; McCree 1 982) . Heichel (1 971 ) showed that the higher
respiration levels occurred in varieties having lower photosynthetic capacity and slower dry matter accumulation. Thus reduction of dark respiration may
improve the carbohydrate balance and ultimately the yield ( Valence et al.
1 984; Gerik and Eastin. 1 985), so genetic variation in maintenance respiration
at high temperature may be useful to screen for high yield or high temperature tolerant lines.
1 .4.2. Thermotolerance of Plants
Usually the term 'stress' may be defined as the exposure of plants to
extraordinarily unfavourable conditions (Larcher 1 980). These responses are
often slight and difficult to detect in supra-/sub-optimal environments. In the case of temperature, active plant growth is generally confined to a temperature
range from 1 0 to 40°C, and temperature extremes above and below this
impose stress on the plant's metabolic activities leading to varied symptoms such as leaf chlorosis, fleck, and scorch; needle blights; stem lesions and
cankers; fruit scald; and finally complete breakdown ( Treshow 1 970).
I
Heat injury is more complex than low temperature injury, since all the reactions in the plant are already taking place rapidly, and a further rise in high temperature might easily disturb the balance. Heat injuries may be divided into direct injury (e.g. disorganization of membrane), indirect injury (e.g. growth
inhibition, starvation, toxicity, biochemical lesions, protein breakdown) and
coincident drought stress injury ( Yarwood 1 961 ; Langride 1 963; Daniel/ et al.
1 969; ltai and Benzioni 1973; Larcher 1 980; Levitt 1 980; Wehner and
Watschke 1 984; Harding et al. 1 989a,b; Lin and Markhart 1 989).
The plant with heat tolerance is able to prevent, decrease or repair heat injury, leading to an increased capacity for survival at extreme temperature ( Crisan 1 973; Larcher 1 980). Thus genotypes having heat tolerance maintain growth under a greater temperature range and show better growth and greater yield at high temperatures (Saadalla et al. · 1 990a). The mechanisms of heat tolerance may involve many adaptations such as, increased protein thermostability leading to prevention of protein denaturation, increased resynthesis of protein to repair heat damage (Brodl 1989; Kimpel et al. 1 990), or alteration of membrane lipid composition leading to improved thermostability (Pearcy 1 978; Santarius and Muller 1 979; Hugly et al. 1 988; Hunst et al. 1 989).
Thermotolerance depends on plant status. Resting (dormant) organisms, such as dry seeds, being able to survive as high as 120°C while in contrast highly hydrated tissues are killed by temperatures as low as 50 - 60°C (Levitt 1 980). The work of Martin and Wehner {1 987) showed that annual bluegrass under frequent watering was heat sensitive, whereas under infrequent irrigation differences appeared. In addition, plants under a low nitrogen application were m ore heat tolerant than those under a high nitrogen application. Annual bluegrass was less tolerant than Kentucky bluegrass at low nitrogen levels but there was no difference at high levels. So the heat tolerance of plants may depend on the surrounding environment and the genotype. Presumably, these ele
�
ated heat tolerances were induced by drought stress or nitrogen deficiency, which may be moderated by abscisic acid (ABA), because these stresses were found to elevate ABA levels (Daie et al. 1 979; Bray 1 988), leading to cross-adaptation (Boussiba et al. 1 975).1 .4.3. Thermotolerance Adaptation
Adaptation is important to prevent injury by a stress which injures the unadapted organism. Plant response to heat stress by rapid adaptation can take place within hours, so that resistance is higher in the afternoon than in the m orning. The enhanced heat adaptation disappears within a few days. The molecular mechanism of adaptation to heat is probably based chiefly on changes in the conformation of protein compounds and stabilization of the
structure of macromoleeular and biomembranes (Larcher 1 980). For instance,
plants grown at low temperature (4°C) ·reach optimum protein synthesis at
27 .5°C, whereas plants kept at 36°C have the highest rate of protein synthesis
at 35°C (Weidner and Zeimens 1 975). Therefore the plant response to heat
tolerance depends on heat acclimation (Saadalla et al. 1 990a). Elevated ABA
levels during heat acclimation may also be involved in heat tolerance (ltai et
a l. 1 978; O'Connor et al. 1 991 ).