β-Cyclocitral Does Not Contribute to Singlet Oxygen-Signalling in Algae, but May Down-Regulate Chlorophyll Synthesis.

Light stress signalling in algae and plants is partially orchestrated by singlet oxygen (O), a reactive oxygen species (ROS) that causes significant damage within the chloroplast, such as lipid peroxidation. In the vicinity of the photosystem II reaction centre, a major source of O, are two β-carotene molecules that quench O to ground-state oxygen. O can oxidise β-carotene to release β-cyclocitral, which has emerged as a O-mediated stress signal in the plant . We investigated if β-cyclocitral can have similar retrograde signalling properties in the unicellular alga . Using RNA-Seq, we show that genes up-regulated in response to exogenous β-cyclocitral included (), while down-regulated genes included those associated with porphyrin and chlorophyll anabolism, such as tetrapyrrole-binding protein (), magnesium chelatases (, , , ), light-dependent protochlorophyllide reductase (), copper target 1 protein (), and coproporphyrinogen III oxidase (). Down-regulation of this pathway has also been shown in β-cyclocitral-treated , indicating conservation of this signalling mechanism in plants. However, in contrast to , a very limited overlap in differential gene expression was found in β-cyclocitral-treated and O-treated . Furthermore, exogenous treatment with β-cyclocitral did not induce tolerance to O. We conclude that while β-cyclocitral may down-regulate chlorophyll synthesis, it does not seem to contribute to O-mediated high light stress signalling in algae.