Search

Light-dependent quenching of room-temperature chlorophyll fluorescence associated with the “energisation” of the thylakoid membrane is usually referred to as qE; improvements in the analysis of chlorophyll fluorescence yield (1,2) allow its quantification. qE is generally taken to reflect an increase in energy dissipation by non-radiative pathways (heat) at Photosystem 2. This increased dissipation has been implicated in the control of electron transport through PS2 (3,4) and in protection of PS2 reaction centres against photoinhibition (5). However, the mechanistic links between the onset of ΔpH and the increased energy dissipation remain obscure.

Photoinhibition of higher plants encompasses a range of phenomena, many of which stem from the requirement to harmlessly dissipate excess light energy. These responses to light stress are manifest as a decrease in the quantum yield of photosynthesis and a quenching of chl fluorescence and primarily affect PS II. In intact plants a number of processes have been suggested to protect the photosynthetic apparatus from the potentially harmful effects of excessive light when dissipation through photosynthesis itself is exceeded. These include ΔpH [1], phosphorylation [2] and the xanthophyll cycle [3]. When the capacity of these processes is exceeded direct damage to a component or components involved in the photochemistry of PS II takes place [4,5,6].

With increasing incident light the efficiency of photosynthesis (Φs = rate of photosynthetic O2 evolution/incident light intensity) tends to decrease. As processes beyond photosystem 2 (PS2) become rate limiting, QA becomes progressively reduced, such that PS2 centres are no longer able to carry out charge separation (closed centres). This is observed as a decrease in the coefficient of fluorescence quenching by photochemistry, qQ, which indicates the proportion of excitation energy delivered to PS2 centres that is captured by ‘open’ centres. Unless a limitation develops at PS2 itself Φs should decrease in proportion to qQ. However it has been found that this is not the case in vivo, and that the parameter Φp (= Φs/qQ), considered to reflect intrinsic quantum yield of PS2, decreases with increasing incident light [1,2]. It has been suggested that this decrease in Φp is related to the non-photochemical dissipation of excitation observed as fluorescence quenching (qNP) [1,2]. In this paper we describe work carried out to determine the mechanism of Φp changes by studying in vitro systems. Although we observe changes in Φp directly related to qNP, we also confirm the observation of Oxborough and Horton [3] that Φp changes can be observed independently of qNP.