Photosystem II Heterogeneity

Abstract

SummaryTwo main topics are addressed in this chapter:’ static heterogeneities’ of PS II, as they appear in standard dark-adapted material, and ‘dynamic heterogeneities’ possibly involved in the non-photochemical quenching processes that modulate the steady-state yield of PS II. Three types of static heterogeneities and possible correlations between them are discussed: (i) Granal and stromal PS II. A fraction, around 10–15%, of the PS II complex is found in stroma lamellae. (ii) PS II α and β. A fraction, around 35%, of PS II (β) appears to have a smaller antenna size and to be organized in isolated units, in contrast with the major part of PS II (α). (iii) A fraction, around 15%, of PS II centers are blocked on the acceptor side (non QE-transferring) and thus inactive with regard to oxygen evolution. A unifying model has been proposed by Melis (1985,1991), wherein stromal PS II, PS IIβ and inactive centers represent essentially the same sub-population of PS II, assumed to reflect a dynamic stock in the biosynthetic turnover of the PS II complex. The various correlations implied by this model are reexamined and evaluated in light of the currently available data, and alternative interpretations are discussed. It is argued that inactive centers belong to PS IIα and that, on the other hand, stromal PS II centers are active. The antenna size of stromal PS II is probably consistent with their belonging to PS IIβ but the amount of the latter exceeds significantly that of stromal PS II: it is suggested that a significant part of PS IIα may be located in the grana margins. The concept of non-photochemical quenching ‘qN’ covers three different contributions. ‘qT’, that appears at low irradiance levels, is interpreted as a ‘state 2 transition’, involving detachment of a fraction of LHCII from PS II α and thus probably increasing the β-fraction ‘qE’, controlled by the lumenal pH, is the major contribution to non-photochemical quenching at physiological irradiances. Most of the available evidence supports its interpretation as due to a dissipation pathway at the antenna level. The alternative mechanism of a formation of inactive centers of the quenching sink type does not account for the results obtained in vivo in normal materials, but seems to prevail in LHCII-deficient material. At over-saturating intensities, the ‘qI’ quenching reflects photoinhibition associated with inactivation of PS II centers in a quenching sink state. Significant formation of non QR-transferring centers does not take place as a result of photodegradation or of blocking the synthesis of the PS II complex. At physiological irradiances, there is no evidence that a sub-population of damaged PS II centers could be ascribed to insufficient synthetic turnover of the PS II complex.