Abstract
When oxygenic photosynthetic organisms are exposed to excessive light and/or heat, Photosystem II is damaged and electron transport is blocked. In these events, reactive oxygen species, endogenous radicals and lipid peroxidation products generated by photochemical reaction and/or heat cause the damage. Regarding light stress, plants first dissipate excessive light energy captured by light-harvesting chlorophyll protein complexes as heat to avoid the hazards, but once light stress is unavoidable, they tolerate the stress by concentrating damage in a particular protein in photosystem II, i.e., the reaction-center binding D1 protein of Photosystem II. The damaged D1 is removed by specific proteases and replaced with a new copy produced through de novo synthesis (reversible photoinhibition). When light intensity becomes extremely high, irreversible aggregation of D1 occurs and thereby D1 turnover is prevented. Once the aggregated products accumulate in Photosystem II complexes, removal of them by proteases is difficult, and irreversible inhibition of Photosystem II takes place (irreversible photoinhibition). Important is that various aspects of both the reversible and irreversible photoinhibition are highly dependent on the membrane fluidity of the thylakoids. Heat stress-induced inactivation of photosystem II is an irreversible process, which may be also affected by the fluidity of the thylakoid membranes. Here I describe why the membrane fluidity is a key to regulate the avoidance and tolerance of Photosystem II on environmental stresses.
Highlights
When oxygenic photosynthetic organisms are exposed to excessive light and/or heat, Photosystem II is damaged and electron transport is blocked
Plants first dissipate excessive light energy captured by light-harvesting chlorophyll protein complexes as heat to avoid the hazards, but once light stress is unavoidable, they tolerate the stress by concentrating damage in a particular protein in photosystem II, i.e., the reaction-center binding D1 protein of Photosystem II
It was demonstrated that lipid peroxide-related substances as well as ROS are produced in the thylakoids by the moderate heat stress, and they have been thought to be responsible for the protein aggregation as described below (Chan et al, 2012)
Summary
Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan. Relocation and/or reorientation of LHCII and PSII complexes take place in the thylakoid membranes in order to decrease energy transfer from LHCII to PSII core (Goral et al, 2010; Herbstova et al, 2012; Yamamoto et al, 2014) These molecular rearrangements upon strong illumination can make the excessive excitation energy captured in LHCII dissipate as heat, and in this respect, reversible aggregation of LHCII plays an important role (Horton et al, 1991; Niyogi, 1999). Abundant and active movement of PSII and LHCII is necessary (Yamamoto et al, 2013; Kirchhoff, 2014; Yamamoto et al, 2014)
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