However this result can be ascribed to an indirect effect, linked to an inability of the CSK mutant to regulate the synthesis of photosynthetic complexes in response to changes in environmental conditions. As a complete interpretation of the steady-state fluorescence emission in presence of actinic background is complicated by the presence of many different physiological processes, we investigated the effect of CSK in the control of state-transitions by fluorescence emission spectroscopy at 77 K of isolated thylakoids. Spectra are shown in Figure 2. In all cases, two principal fluorescence emission maxima are seen, one centred at 685 nm, also associated with a shoulder at,700 nm, and arising principally from photosystem II emission and the other, centred at 735 nm, which originates from photosystem I. The intensity of the 685 nm and 735 nm peaks observed at 77 K can be used to estimate the relative absorption cross-section of the two photosystems, and hence on state transitions. The state 2 transition was induced in vitro by BMS-354825 Src-bcr-Abl inhibitor illumination of thylakoids in the presence of ATP, and state 1 was produced from thylakoids incubated in the dark with ATP. As a control, thylakoids were incubated in the dark without ATP, and this treatment also induces state 1. It is seen in all cases that the emission ratio F735/F685 is greater in state 2 than in state 1, most noticeably in thylakoids from white light-grown plants. However, the effect of the ATP and illumination on excitation energy distribution between photosystems I and II is much the same in the CSK mutant as in the wild-type. Thus, neither the Fm values from white light grown plants at room temperature nor 77 K fluorescence emission spectra indicate any effect of the CSK mutation on redistribution of excitation energy in light-state transitions. Phosphorylation of light harvesting complex II by the LHC II kinase induces state 2 transition, and its dephosphorylation by the phospho-LHC II phosphatase leads to state 1 transition. In order to further probe the role of CSK in state transitions, we carried out a thylakoid phosphorylation assay for the CSK mutant and the wild-type. Thylakoids were first isolated from white light grown plants, and incubated in light for 10 minutes in the presence of ATP. The results of 32Plabelling experiments are shown in Figure 3. Incubation of thylakoids in white light induces the state 2 transition via phosphorylation of LHC II. Figure 3 shows equal levels of LHC II phosphorylation in both CSK mutant and wild type. In the light, the electron transport inhibitor 3–1,1-dimethylurea inhibits electron transport to plastoquinone and makes the plastoquinone pool oxidised. Oxidised plastoquinone promotes the state 1 transition, and LHC II remains in an unphosphorylated state. Thus, incubation of wild-type and CSK mutant thylakoids with DCMU in the presence of light abolishes 32Plabelling of LHC II. Dark-incubated thylakoids are in state 1, as the plastoquinone pool is usually oxidised in the dark, but state 2 can be induced in dark-incubated thyalkoids by the addition of the reducing agent sodium dithionite. Incubation of thylakoids in the dark in the presence of sodium dithionite results in phosphorylation of LHC II.