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SUSCEPTIBILITY AND PROTECTIVE MECHANISMS OF MOTILE AND NON MOTILE CELLS OF HAEMATOCOCCUS PLUVIALIS (CHLOROPHYCEAE) TO PHOTOOXIDATIVE STRESS1
Article first published online: 10 MAY 2012
© 2012 Phycological Society of America
Journal of Phycology
Volume 48, Issue 3, pages 693–705, June 2012
How to Cite
Han, D., Wang, J., Sommerfeld, M. and Hu, Q. (2012), SUSCEPTIBILITY AND PROTECTIVE MECHANISMS OF MOTILE AND NON MOTILE CELLS OF HAEMATOCOCCUS PLUVIALIS (CHLOROPHYCEAE) TO PHOTOOXIDATIVE STRESS. Journal of Phycology, 48: 693–705. doi: 10.1111/j.1529-8817.2012.01147.x
Received 20 April 2011. Accepted 8 December 2011.
- Issue published online: 1 JUN 2012
- Article first published online: 10 MAY 2012
- Accepted manuscript online: 22 MAR 2012 11:25AM EST
- Haematococcus pluvialis;
- motile cell;
- nonmotile cell;
- photooxidative stress
The life cycle of the unicellular green alga Haematococcus pluvialis consists of motile and nonmotile stages under typical growing conditions. In this study, we observed that motile cells were more susceptible than nonmotile cells to high light, resulting in a decrease in population density and photo-bleaching. Using two Haematococcus strains, CCAP 34/12 (a motile cell dominated strain) and SAG 34/1b (a nonmotile cell dominated strain), as model systems we investigated the cause of cell death and the protective mechanisms of the cells that survived high light. The death of motile cells under high light was attributed to the generation of excess reactive oxygen species (ROS), which caused severe damage to the photosynthetic components and the membrane system. Motile cells were able to dissipate excess light energy by nonphotochemical quenching and to relax ROS production by a partially up-regulated scavenging enzyme system. However, these strategies were not sufficient to protect the motile cells from high light stress. In contrast, nonmotile cells were able to cope with and survive under high light by (i) relaxing the over-reduced photosynthetic electron transport chain (PETC), thereby effectively utilizing PETC-generated NADPH to produce storage starch, neutral lipid, and astaxanthin, and thus preventing formation of excess ROS; (ii) down-regulating the linear electron transport by decreasing the level of cytochrome f; and (iii) consuming excess electrons produced by PSII via a significantly enhanced plastid terminal oxidase pathway.