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Alleviation of heat damage to photosystem II by nitric oxide in tall fescue.

Research paper by Ke K Chen, Liang L Chen, Jibiao J Fan, Jinmin J Fu

Indexed on: 09 Jul '13Published on: 09 Jul '13Published in: Photosynthesis Research



Abstract

Nitric oxide (NO) has been found to mediate plant responses to heat stress. The objective of this study was to investigate the protective role of NO in the recovery process of photosystem II (PSII) in tall fescue (Festuca arundinacea) against heat stress. Treatment of tall fescue leaves with NO donor sodium nitroprusside significantly improved the overall behavior of PSII probed by the chlorophyll a fluorescence transients, while the inhibition of NO accumulation by 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (PTIO, a NO scavenger) plus N (G)-nitro-L-arginine-methyl ester (L-NAME, NO synthase inhibitor) dramatically disrupted the operation of PSII. Specifically, under heat stress, the exogenous NO reduced the initial fluorescence (F 0), increased the maximal quantum yield (F V/F M), and disappeared the K-step of 0.3 ms. By the analysis of the JIP-test, the exogenous NO improved the quantum yield of the electron transport flux from Q A to Q B (ET0/ABS), and decreased the trapped excitation flux per reaction center (RC) (TR0/RC), electron transport flux per RC (ET0/RC), and electron flux reducing end electron acceptors per RC (RE0/RC). In addition, the exogenous NO reduced the content of H2O2, O 2 (•-) , and malondialdehyde and electrolyte leakage of tall fescue leaves. These data suggest that exogenous NO could protect plants, increase the amount of activated RC and improve the electron transport from oxygen evolving complex to D1 protein. Moreover, quantitative RT-PCR revealed that, in the presence of hydrogen peroxide, NO induced the gene expression of psbA, psbB, and psbC, which encode proteins belonging to subunits of PSII core reaction center (Psb) complex. These findings indicate that, as an important strategy to protect plants against heat stress, NO could improve the recovery process of PSII by the up regulation of the transcriptions of genes encoding PSII core proteins.