Cytokinin-induced photosynthetic adaptability of Zea mays L. to drought stress associated with nitric oxide signal: Probed by ESR spectroscopy and fast OJIP fluorescence rise

Nitric oxide (NO), as a diffusible molecule, performs important roles in diverse physiological processes. Interestingly. NO signaling is based on interactions with plant hormones. The aim of this study was, first, to test the effect of cytokinin (CTK) on the primary reaction of photosynthesis under drought stress, and then to examine whether NO is involved in CTK-induced photosynthetic resistance due to its role as a second messenger in stress response. Under drought stress, plants were treated with CTK, or CTK plus the NO scavenger (Hemoglobin [Hb]) for 6 h. The effects of CTK and Hb on fast OJIP fluorescence rise were then examined. At the same time, NO and reactive oxygen species (ROS) signals in all the treatments were detected by electron spin resonance (ESR) spectroscopy. The results showed that CTK-regulated fluorescence transient rise under drought stress and increased the electron donation capacity of photosynthesis system (PS) II. The plant photosynthetic performance index (PI) on an absorption basis and corresponding three PI components (RC/ABS, P-TR, and P-ET) also increased. High NO signal intensity alleviated drought-induced ROS damage to plants; thus, the signal probably played a direct role in eliciting CTK regulation to energy absorption (RC/ABS) and excitation energy trapped (P-TR) in response to drought. Although CTK stimulated more excitation energy conversion to electron transfer (P-ET), because NO was probably bound to the plastoquinone pool (PQ) of the electron transport chain, CTK decreased electron transport to the acceptor side of PSII (see V-1, Sm and N). Furthermore, CTK stimulated more NO signal formation, probably mainly via a nitrate reductase (NR) source under the conditions of the study, and Hb prevented stimulation from CTK. However, these results will require confirmation from future studies. Crown Copyright (C) 2009 Published by Elsevier GmbH. All rights reserved.