engleski

Thylakoid FNR-TROL complex is a source of metabolic retrograde signalling

We have recently described TROL (thylakoid rhodanese-like protein), a nuclear-encoded component of thylakoid membranes that is required for tethering of FNR and sustaining efficient linear electron flow (LEF) in vascular plants. TROL consists of two distinct modules ; a centrally positioned rhodanese-like domain and a C-terminal hydrophobic FNR binding region. Analysis of Arabidopsis mutant lines indicates that in the absence of TROL relative electron transport rates at high-light intensities are severely lowered accompanied with significant increase in non-photochemical quenching (NPQ). Depletion of TROL causes anatomical, as well as ultrastructural changes at the level of chloroplast structure. The observed changes prompted us to investigate alterations in global gene expression patterns. A total number of 237 differentially expressed genes were selected according to q-value < 0.001 cutoff. To demonstrate the biological meaning of the observed changes, from this set of genes those encoding chloroplast-targeted proteins were further selected. Among up-regulated genes are POR B, which uses NADPH for chlorophyll biosynthesis, and the malate-valve enzyme NADP-malate dehydrogenase (MDH), which potentially generates NADPH in an alternative pathway. It is possible that TROL deficiency negatively influences NADPH synthesis, which plants try to compensate by redirecting the NADPH synthesis pathway from FNR to the MDH. Furthermore, modulation of genes involved in biosynthesis and trafficking of tocopherol, as well as, DNAJ protein, thioredoxin, and glutathione-S-transferase indicates that TROL deficient plants might use metabolic retrograde signalling to adapt their responses to oxidative stress.

Chloroplast; Photosynthesis; Redox-regulation; NPQ

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