Nitric Oxide Down-Regulation of Carotenoid Synthesis and PSII Activity in Relation to Very High Light-Induced Singlet Oxygen Production and Oxidative Stress in Chlamydomonas reinhardtii.

Plant & cell physiology

PubMedID: 23713096

Chang HL, Hsu YT, Kang CY, Lee TM. Nitric Oxide Down-Regulation of Carotenoid Synthesis and PSII Activity in Relation to Very High Light-Induced Singlet Oxygen Production and Oxidative Stress in Chlamydomonas reinhardtii. Plant Cell Physiol. 2013;54(8):1296-315.
Nitric oxide (NO) was produced in Chlamydomonas reinhardtii cells 30 min after illumination at a very high light intensity of 3,000 ┬Ámol m(-2) s(-1) (VHL) followed by singlet oxygen ((1)O2) production, lipid peroxidation, expression of oxidative stress-related genes, irreversible PSII inactivation and cell death. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), an NO scavenger, effectively reduced (1)O2 levels and VHL damage, while treatment with diphenylamine (DPA), an (1)O2 scavenger, only slightly reduced NO levels, though VHL damage was still effectively reduced. In the presence of cPTIO, the decline in minimum (Fo, Ft) and maximum (Fm, Fm') fluorescence after 60 min of VHL illumination can be slowed, and after recovery to 50 ┬Ámol m(-2) s(-1) conditions, PSII activity (Fv/Fm, Fv'/Fm') and PSII donor-side and acceptor-side electron transfer were partially restored. This finding indicates that (1)O2 production is induced by NO through inhibition of PSII electron transfer under VHL conditions. VHL illumination caused a decrease in carotenoid contents but a transient increase in the transcription of two enzymes involved in carotenoid synthesis, phytoene synthase (PSY) and phytoene desaturase (PDS), at 30 min followed by a decrease at 60 min. The VHL-induced decrease in PDS transcription can be inhibited in the presence of cPTIO. The results of the present study show that NO generated in C. reinhardtii cells under VHL conditions induces (1)O2 accumulation due to a decrease in the (1)O2-scavenging capacity caused by NO-mediated inhibition of carotenoid synthesis and PSII electron transport, which, in turn, leads to oxidative damage and cell death.