Physiology and Molecular Biology of Stress ... - KHAM PHA MOI

High Temperature Stress
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Manganese is an essential element of the water splitting complex of PSII,
which oxidizes water and transfers the resulting electrons to P680. Therefore, the
observed loss of manganese during inhibition of O 2
evolution suggests that heat is
destroying the Mn complex. However, immobilization of the 33 kDa protein of PSII
stabilized the water splitting complex and prevented the loss of Mn during heat stress
(Enami et al., 1994b). Further, these studies showed that O 2
evolution could be completely
inhibited by heat stress while 80% of Mn remained bound to PSII, suggesting
the requirement of both Mn and the 33 kDa protein for O 2
evolution. The 33 kDa protein
is a thermally stable protein, although its secondary structure is affected by heat stress,
which dissociates from PSII upon heating (Enami et al., 1994a; Lydakis-Simantiris et al.,
1999). Upon cooling, a portion of the 33 kDa proteins reassociate with PSII. This
accounts for the observed partial recovery of O 2
evolution after heat stress. Pueyo et
al. (2002) also demonstrated that the thermal stability of O 2
evolution in spinach could
be enhanced by substitution of the native 33 kDa protein with a homologue from the
thermophilic cyanobacterium Phormidium laminosum that has a more thermally stable
protein secondary structure. This suggests that the thermal stability of the secondary
structure of the 33 kDa protein is important for binding with PSII under heat stress
conditions.
Although inhibition of O 2
evolution was the earliest noted effect of heat on
PSII, high temperature also blocks the reaction center of PSII and causes a dissociation
of the light harvesting pigment from the reaction center (Schreiber and Armond, 1978).
While electron transport could be restored in heat damaged PSII using electron donors,
other studies noted that full recovery of electron transport could not be obtained after
heating with electron donors that supplied electrons before plastoquinone, suggesting
further damage to PSII apart from the dissociation of the water splitting complex
(Yamashita and Butler, 1968). This thermal blocking of the reaction center of PSII has
been attributed to either a slowed rate of electron flow from Q A
- to Q B
or a back flow of
electrons from Q B
- to Q A
using triazine resistant plants (Ducruet and Lemoine, 1985;
Ducruet and Ort, 1988; Havaux, 1989; Ducruet, 1999) and in Amaranthus chloroplasts
(Bukhov et al., 1990). Further, Egorova et al. (2003) showed that the reduction of
plastoquinone by stromal reductants during heat stress caused a back pressure of
electrons on PSII thus causing a reduction of Q A
by Q B
-. This strongly suggests that
the thermal blocking of PSII noted first by Schreiber and Armond (1978) is due to the
reduction of plastoquinone from stromal sources.
The dissociation of the light harvesting pigment from the reaction center during
heat stress has been attributed to the disconnection of the LHCII complexes from
the functional core of PSII. Several freeze fracture studies have shown a decrease in
particle size located in the thylakoid membranes after heat stress, indicating a physical
separation of the LHCII complexes from the core of PSII (Armond et al., 1980; Gounaris
et al., 1983, 1984). This dissociation is further linked to either a state I to state II
transition in leaves heated to 42°C or to the formation of aggregates of LHCII complexes
in the thyalkoid membranes in leaves heated to 45°C and above (Pastenes and Horton,