LHCSR3-dependent quenching in photosystem II supercomplex of Chlamydomonas reinhardtii

Eunchul Kima, Ryutaro Tokutsua, Makio Yokonob, Seiji Akimotoc, Jun Minagawaa
aDivision of Environmental Photobiology, National Institute for Basic Biology, Okazaki 444-8585, Japan; bInstitute of Low Temperature Science, Hokkaido University, Sapporo 060-0819, Japan; cMolecular Photoscience Research Center, Kobe University, Kobe 657-8501, Japan

Non-photochemical quenching (NPQ), which is a photoprotective mechanism, in photosynthetic organisms has been intensively studied in a recent decade. Recently, LHCSR3 (Light-harvesting complex stress related 3) has been discovered as a key player for the photoprotective energy dissipation in Chlamydomonas reinhardtii (Peers et al. 2009). LHCSR3 is expressed under high-light conditions and regulates NPQ in Chlamydomonas reinhardtii (Peers et al. 2009), and following reconstitution study have revealed that LHCSR3 is a pigment-binding protein and has two functions as a quencher and pH-sensor (Bonente et al. 2011). The high levels of carotenoid (Car) radical cations and the fast chlorophyll (Chl) fluorescence lifetime component of LHCSR3 indicate multiple mechanisms, such as Chl-Car charge transfer (Holt et al. 2005; Ahn et al. 2008), direct energy transfer from Chl a Qy transition to a lutein S1 state (Ruban et al. 2007) and Chl-Chl charge transfer (Muller et al. 2010), are involved in LHCSR3-induced quenching. Meanwhile, Tokutsu and Minagawa have isolated PSII-LHCII-LHCSR3 supercomplexes and investigated its LHCSR3-dependent quenching at acidic pH (Tokutsu and Minagawa 2013). However, the details on the mechanism how LHCSR3 enhance energy dissipation ability in PSII supercomplex have not been studied yet. In this study, ultrafast spectroscopy has been applied to investigate the mechanism of LHCSR3-induced quenching in PSII supercomplexes.