Abstract
Non-photochemical quenching (NPQ) helps dissipate surplus light energy, preventing formation of reactive oxygen species (ROS). In Chlamydomonas reinhardtii, the thylakoid membrane protein LHCSR3 is involved in pH-dependent (qE-type) NPQ, lacking in the npq4 mutant. Preventing PSII repair revealed that npq4 lost PSII activity faster than the wild type (WT) in elevated O2, while no difference between strains was observed in O2-depleted conditions. Low Fv/Fm values remained 1.5 h after moving cells out of high light, and this qH-type quenching was independent of LHCSR3 and not accompanied by losses of maximum PSII activity. Culturing cells in historic O2 atmospheres (30-35%) increased the qE of cells, due to increased LHCSR1 and PsbS levels, and LHCSR3 in the WT, showing that atmospheric O2 tensions regulate qE capacity. Colony growth of npq4 was severely restricted at elevated O2, and npq4 accumulated more reactive electrophile species (RES) than the WT, which could damage PSI. Levels of PsaA (PSI) were lower in npq4 grown at 35% O2, while PsbA (PSII) levels remained stable. We conclude that even at high O2 concentrations, the PSII repair cycle is sufficient to maintain net levels of PSII. However, LHCSR3 has an important function in protecting PSI against O2-mediated damage, such as via RES.
Highlights
Molecular oxygen is a photosynthetic by-product from the water-splitting activity of PSII
Chlamydomonas reinhardtii mutants affected in Non-photochemical quenching (NPQ) with their corresponding wild type (WT), WT-cw15 and WT-4A, as well as WT-D66, were screened for the effect of elevated O2 on growth and qE
We showed that O2 availability influences how important qE is in protecting the photosynthetic apparatus from photoinhibition, and that in C. reinhardtii the O2 tension is a regulator of qE capacity
Summary
Molecular oxygen is a photosynthetic by-product from the water-splitting activity of PSII. O2 forms unstable radical and non-radical reactive oxygen species (ROS), and the initial accumulation of O2 is thought. LHCSR3 prevents O2-dependent photoinhibition of PSI and PSII | 2651 to have caused the first major extinction event of our planet (Lane, 2002). Photosynthesis is a major source of ROS that have to be dealt with (Halliwell, 2006), especially in response to increasing light intensity (Roach et al, 2015a). At lower and more typical physiological levels, 1O2 peroxidizes membrane lipids, which break down and release aldehydes that include reactive electrophile species (RES), such as acrolein (Fischer et al, 2012; Mano, 2012; Roach et al, 2017;Yalcinkaya et al, 2019). Photoinhibition of PSI is a very costly process for the plant since no fast repair cycle exists (Sonoike, 2011). The 4Fe4S clusters FA, FB, and Fx have been identified as the site of damage in PSI (Sonoike et al, 1995;Tiwari et al, 2016)
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