Skip to main content
. 2017 Sep 22;13(9):e1007022. doi: 10.1371/journal.pgen.1007022

Fig 1. Inhibitors and mechanisms modulating metabolic flux to isoprenoids in chloroplasts.

Fig 1

(A) Schematic representation of: (1) MEP pathway and derived products, with the position of enzymes (DXS, DXR) and inhibitor (FSM, NFZ) targets; (2) Hsp70-dependent pathways for misfolded and aggregated forms of DXS to be degraded (via ClpC1 and the Clp protease) or, alternatively, reactivated (via ClpB3); and (3) proposed mechanism by which interference with PGE (e.g. with LIN) impacts the activity of the Clp protease complex, based on the production of the plastome-encoded ClpP1 subunit. Red arrow represents the stress-induced refolding pathway. Dashed arrows represent multiple steps. GAP, glyceraldehyde 3-phosphate; DXP, deoxyxylulose 5-phosphate. See text for other acronyms. (B) Quantification of the inhibitor resistance phenotype estimated from chlorophyll levels in the absence (100%) or presence of inhibitors. (C) Representative images of Arabidopsis WT (Columbia) seedlings germinated and grown for 10 days under LD in the presence of the indicated concentrations of inhibitors.