220-229Exposure o f isolated thylakoids or intact plants to
elevated temperature is known to inhibit photosynthesis at multiple sites. We
have investigated the effect of elevated temperature (40°C) for 24 hr in dark
on rice seedlings to characterize the extent of damage by inl vivo heat
stress on photofunctions of photosystem II (PSII). Chi a fluorescence
transient analysis in
the intactrice leaves indicated a loss in PSII
photochemistry (Fv) and an associated loss in the number of functional
PSII units. Thylakoids isolated from rice seedlings exposed to mild heat stress
exhibited > 50% reduction in PSII catalyzed oxygen evolution activity
compared to the corresponding control thylakoids. The ability of thy lakoid
membranes from heat
exposed seed lings to photooxidize artificial PSII electron
donor, DPC, subsequent to washing the thylakoids with alkaline Tris or NH2OH
was also reduced by ~40% compared to control Tris or NH2OH washed
thylakoids. This clearly indicated that besides the disruption of oxygen
evolving complex (OEC) by 40°C heat exposure for 24 hr, the PSII reaction
centers
were impaired by inl vivo heat stress. The analysis
of Mn and manganese stabilizing protein (MSP) contents showed no breakdown of
33 kDa extrinsic MSP and only a marginal loss in Mn. Thus, we suggest that the
extent of heat induced loss of OEC must be due to disorganization of the OEC
complex by in vivo heat stress. Studies with inhibitors like DCMU and
atrazine clearly indicated that in vivo heat
stress altered the acceptor side significantly. [14C] Atrazine
binding studies clearly demonstrated that there is a significant alteration in
the QB binding site on D1 as well as altered QA to QB
equilibrium. Thus, our results show that the loss in PSII photochemistry by in
vivo heat exposure not only alters the donor side but significantly alters
the acceptor side of PSII .</span