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

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T.D. Sharkey and S.M. Schrader
phosphorylation of LHCII and state transitions and a second system that controls
phosphorylation/dephosphorylation of the other thylakoid proteins. A large number
of thylakoid proteins undergo reversible phosphorylation (Hansson and Vener, 2003)
and heat stress is one of the most effective ways of modulating the phosphorylation
status of many of them (Vener et al., 2001). For some thylakoid proteins whose phosphorylation
status varies, the function of the protein is not known (Carlberg et al., 2003;
Hansson and Vener, 2003).
One of the processes in which phosphorylation plays a role is repair of damaged
D1 proteins. PSII complexes with a damaged D1 migrate from the stacked to
unstacked thylakoids for repair, but the D1 has to be dephosphorylated before the
repair can occur (Rintamäki et al., 1996). Migration and dephosphorylation of D1 are
reduced at low temperature, which could explain why unsaturation of thylakoid lipids,
which is deleterious at high temperature (Kunst et al., 1989; Murakami et al., 2000), is
advantageous at low temperature (Vijayan and Browse, 2002). When the membrane is
too rigid, PSII particles cannot migrate to the unstacked thylakoids as needed for repair.
3.3.5. Thermoprotection
Heat stress clearly causes a decline in the carbon assimilation of photosynthesis, but it
is not certain what the primary cause of this observed decline is. Three components of
the photosynthetic machinery have been suggested to be the primary heat labile component:
PSII, lipid permeability, and rubisco activase. The other observed phenomenon
during heat stress can be seen as protective mechanisms designed to protect
either PSII or the lipid membrane. No protective mechanisms aside from a modified
enzyme have been shown for rubisco activase. Further, several mechanisms have been
shown to increase thermal stability in photosynthesis that are not directly involved
with the conversion of light energy or the fixation of CO 2
.
Much of the protection of PSII and the lipid membranes seems to center on
cyclic electron transport. The induction of cyclic electron transport during heat stress
would explain many observed phenomenon including the stimulation of PSI while PSII
is inhibited, the reduction of the intersystem electron transport chain by stromal reductants
and the subsequent blocking of the PSII reaction center, the state I to state II
transition, the acidification of the lumen while the lipid membrane becomes progressively
leakier, and the subsequent increase nonphotochemical quenching, qN. The
protection provided by cyclic electron transport resides in the formation of the ionic
gradient across the thylakoid membrane and nonphotochemical quenching (Horton et
al., 1996). It is beyond the scope of this review to discuss the mechanisms of
nonphotochemical quenching, but a review of its importance with heat stress is discussed.
Interestingly, if the formation of a high pH gradient across the thylakoid
membranes is protective during heat stress, then the deactivation of rubisco may be an
adaptive response rather than maladaptive.