Figure 6.

ftsh1-1 Increases PSII Sensitivity to Photoinhibition, Prevents PSII Repair, and Leads to the Accumulation of D1 Fragments.

(A) Time course of photoinhibition at 250 μE m⁻² s⁻¹ and recovery at 6 μE m⁻² s⁻¹ in wild-type and ftsh1-1 strains in the absence or presence of inhibitors of the translation of chloroplast genes (500 μg mL⁻¹ lincomycin and 100 μg mL⁻¹ chloramphenicol [LC]) as monitored by PSII activity (F_v/F_m). The inset shows kinetics of the PSII activity loss upon photoinhibition in an independent experiment.

(B) D1 model with the localization of the D1 DE loop and C-terminal peptides recognized by antibody (adapted from Kapri-Pardes et al., 2007).

(C) Time course of photoinhibition and recovery in wild-type and ftsh1-1 strains as monitored by levels of D1 and D1 fragments immunodetected with D1 DE loop and C-terminal antibodies using the PSII OEE2 extrinsic subunit as a loading control. Total cell proteins were separated by SDS/urea-PAGE.