LHCSR (LI818) has an important role in conferring high light resistance to a Chlamydomonas reinhardtii mutant

Nandini S. Bhogar1, Britta Förster2, Barry Pogson2, and Dion G. Durnford1

1) University of New Brunswick, Fredericton, Canada 2) Australian National University, Canberra, Australia

Damage to the photosynthetic apparatus occurs when absorbed light energy exceeds the photosynthetic capacity to utilize it. Short-term mechanisms, such as non-photochemical quenching (NPQ) and state transitions, attempt to compensate and prevent photodamage, but often long-term photoacclimation mechanisms are required for a prolonged stress. In C. reinhardtii, a gain-of-function mutant resistant to very high light (VHLR-S9) grows faster, has higher zeaxanthin levels and generates lower levels of reactive oxygen species under high-light stress compared to the wild-type (Förster et al., 2005. Biochem. Biochim. Acta 1709: 45-57). The mechanisms underlying its ability to tolerate very high light remains largely unknown. In an effort to further examine the basis of the VHLR phenotype, we examined the induction of a distant member of light-harvesting complex protein family, LHCSR. The VHLR-S9 mutant over-expresses LHCSR under all light conditions, whereas in the wild-type its induction is primarily associated with high-light exposure. In this study, we examined the NPQ induction in the wild-type and VHLR-S9 mutant under a variety of conditions and found the NPQ capability correlated with LHCSR protein abundance. This agrees with a recent report showing a LHCSR has a role in NPQ in Chlamydomonas (Peers et al., 2009. Nature 462:518-21) and suggests that high light resistance of VHLR-S9 is due, in part, to enhanced NPQ from LHCSR over-expression.

e-mail address of presenting author: m6432@unb.ca