Abstract

The molecular defense mechanisms against photooxidative stress in photosynthetic organisms are essential to protect cells from damaging effects of high light illumination and photoinhibition but also to protect against effects by endogenous and exogenous photosensitizers. Here, we analyzed the genetic response of Chlamydomonas reinhardtii to the model type I photosensitizer neutral red (NR) and the type II photosensitizer rose bengal (RB) using DNA-microarrays. Many oxidative and general stress response genes, which were also induced by other oxidative stress conditions, were strongly induced by NR. Only one gene was upregulated by RB, the glutathione (GSH) peroxidase homologous gene Gpxh, which was also induced by NR. In addition NR exposure resulted in the reduced expression of most nuclear photosynthetic genes and subunits of the light harvesting complex (LHC) indicating an effect on the photosynthetic activity. This is supported by a stimulation of singlet oxygen generation in NR-treated thylakoids. Thus, in C. reinhardtii the Gpxh expression is most probably induced by the formation of singlet oxygen in both the NR and RB-treated cells via the activation of a very sensitive and specific sensor, whereas general oxidative stress response mechanisms seem to be involved in the response of most other genes to the type I photooxidative stress.

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