Ruban A V, Walters R G, Horton P
Robert Hill Institute, Department of Molecular Biology and Biotechnology, University of Sheffield, UK.
FEBS Lett. 1992 Sep 7;309(2):175-9. doi: 10.1016/0014-5793(92)81089-5.
Non-radiative dissipation of absorbed excitation energy in chloroplast membranes is induced in the presence of the trans-thylakoid proton motive force; this dissipation is measured as high energy state quenching of chlorophyll fluorescence, qE. It has been suggested that this results from a low pH-induced structural alteration in the light harvesting complex of photosystem II, LHCII [(1991) FEBS Letters 292, 1-4]. The effect of the carboxyl-modifying agent, dicyclohexylcarbodiimide (DCCD), on energy dissipation in chloroplast membranes has been investigated. At concentrations below that required to inhibit electron transport, DCCD caused a decrease in the steady state delta pH, completely inhibited qE and also inhibited the low pH-dependent induction of qE. DCCD binding to polypeptides in the 22-28 kDa range correlated with inhibition of qE. It is suggested that DCCD reacts with amino acid residues in LHCII whose protonation is the primary event in the induction of energy dissipation. This LHCII domain may be identical to one forming a proton channel linking the site of PSII-dependent water oxidation to the thylakoid lumen [(1990) Eur. J. Biochem. 193, 731-736].
在类囊体跨膜质子动力存在的情况下，叶绿体膜中吸收的激发能会发生非辐射耗散；这种耗散以叶绿素荧光的高能态猝灭qE来衡量。有人认为，这是由于光系统II捕光复合体LHCII中低pH诱导的结构改变所致[（1991年）《欧洲生物化学学会联合会快报》292，1 - 4]。研究了羧基修饰剂二环己基碳二亚胺（DCCD）对叶绿体膜中能量耗散的影响。在低于抑制电子传递所需浓度时，DCCD导致稳态ΔpH降低，完全抑制qE，并抑制qE的低pH依赖性诱导。DCCD与22 - 28 kDa范围内的多肽结合与qE的抑制相关。有人认为，DCCD与LHCII中的氨基酸残基反应，这些残基的质子化是诱导能量耗散的主要事件。这个LHCII结构域可能与一个形成质子通道的结构域相同，该质子通道将依赖于PSII的水氧化位点与类囊体腔连接起来[（1990年）《欧洲生物化学杂志》193，731 - 736]。
