Photosystem II monomeric antenna CP26 has a key role in Non-Photochemical Quenching inChlamydomonas reinhardtii

Abstract

Eukaryotic photosynthetic organisms have evolved an array of "antenna" complexes where both light harvesting and photoprotective mechanisms occur. Thermal dissipation of the excitation energy harvested in excess, named non-photochemical quenching (NPQ), is one of the main photoprotective mechanisms evolved in eukaryotic organisms to prevent photooxidative stress. Here, the role of the Photosystem II monomeric antenna CP26 was investigated in Chlamydomonas reinhardtii, model organism for green algae, using a genome editing approach to obtain cp26 knock-out mutant strains (named k6). The absence of CP26 caused a reduced growth at low or medium light but not at high irradiances. Photosystem II were partially affected by the absence of CP26 having reduced photochemical efficiency, light harvesting capacity and excitation energy transfer. However, the main phenotype observed in k6 was a strong reduction of NPQ, being reduced by more than 70% compared to wild type. The NPQ phenotype observed was rescued by genetic complementation of k6 mutant demonstrating that ~50% of CP26 content compared to wild type was able to restore the NPQ capacity. The comparison of k6 mutant with mutants deprived of the other Photosystem II monomeric antenna, CP29 or missing both CP26 and CP29, demonstrated that these monomeric antenna proteins have different specific functions in Chlamydomonas reinhardtii: CP26 plays a pivotal role in NPQ induction while the binding of CP29 to Photosystem II is crucial for its photochemical activity. The genetic engineering of these two proteins could be a promising strategy to regulate photosynthetic efficiency of microalgae under different light regimes.