Photoinhibition of photosynthesis in vivo: Involvement of multiple sites in a photodamage process under CO 2- and O 2-free conditions

Abstract

Intact Lemna gibba plants were illuminated by photoinhibitory light in air, in air minus O 2, in air minus CO 2, and in pure N 2. In pure N 2, the degree of photoinhibition increased 3–5-times compared with that in air. This high degree of photoinhibition is described as photodamage. Photodamage was found to constitute a syndrome, that is, it is due to inactivation of multiple sites. These sites include RC II component(s) from P680 to Q A; the Q B-site; and a component of PS I. In photodamage, the donor side of PS II and PS II excitation energy transfer remain unimpaired, but the size of the PS I antenna seems to decrease. Photodamage is distinguishable from photoinactivation. Photoinactivation occurred in air and could be attributed to inhibition of electron transport from Q − A to Q B. During photoinactivation the D1 protein of RC II became degraded faster than the detectable inhibition of Q B reduction. The photoinhibition-induced rise in F 0 occurred only during the process of photodamage but not during that of photoinactivation, and was a secondary event which arose as a consequence of photodamage. Atmospheric O 2 alleviated photodamage but increased photoinactivation. The light-induced D1 degradation and inhibition of Q A to Q B electron transfer were enhanced in vivo not only by O 2 but also by depletion of CO 2.