Genotypic-dependent alternation in D1 protein turnover and PSII repair cycle in psf mutant rice (Oryza sativa L.), as well as its relation to light-induced leaf senescence

Abstract

To clarify the genotypic-dependent alternation in D1 protein turnover and PSII repair cycle and its relation to light intensity in senescent leaves of rice, two rice genotypes, namely, the psf mutant and its wild type, were used to determine their temporal differences in terms of the net photosynthetic rate (Pn), chlorophyll fluorescence parameters of PSII, and transcriptional levels of genes that participated in D1 protein turnover during leaf senescence. The results showed that compared to its wild type, the psf mutant had lower Pn, solar energy transmitting efficiency (Fv/Fm), and performance index on absorption basis (PIabs) than its wild type. Moreover, our results showed that the emergence of leaf senescent symptoms for psf mutant mainly depends on light intensity, instead of light quality in the field. The prevention of leaves from sugar starvation and oxidative damage contributes to the regulation of shaded-delayed leaf senescence in the psf mutant. Both non-phosphorylated and phosphorylated D1 proteins in leaves of the psf mutant were found decreasing with leaf senescence, while the non-phosphorylated one had more decrease. The initiation and subsequent progresses of leaf senescence induced by light were closely related to the D1 protein turnover in the leaves of the psf mutant. Partial shading treatment within an intact leaf concomitantly alleviated or even repaired the leaf premature senescent symptoms of the shaded area, which also suppressed D1 protein from being degraded. The key genes (OsPsbA and OsFtsHs) participated in D1 protein de novo synthesis and PSII repair cycle had lower expression during leaf senescence. Among different OsFtsH isoforms, OsFtsH2 exhibited the highest transcriptional levels, and it was also the isoform gene with the largest decline in the light treatment. Meanwhile, OsFtsH5 and OsFtsH7 were only down-regulated in conditions with high light intensity. Therefore, the inhabitation of D1 de novo synthesis and photo-damaged D1 degradation are mainly due to the down-regulation of OsPsbA and OsFtsH2. Other OsFtsH isoforms may play synergistic or complementary roles in D1 protein turnover and PSII repair cycle in light-induced leaf senescence.