Role of nitric oxide in delaying senescence of cut rose flowers and its interaction with ethylene

Recent studies showed that nitric oxide (NO) functions as an essential endogenous plant signal molecule. In this study, the regulatory role of NO during the flower senescence of cut rose (Rosa hybrida L 'Kardinal') was surveyed. Exogenous application of the NO donor sodium nitroprusside (SNP) could increase vase life and maximum flower diameter and its effects were dose and time dependent. Treatments with 200 mu M of SNP for 24 h obtained the maximum vase life and flower diameter. NO scavengers 2-(4-carboxy2-phenyl)-4,4, 5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or methylene blue (MB-1) and NO synthase (NOS) inhibitors N-nitro-L-arginine methyl ester (L-NAME) or S,S'-1,3-phenylene-bis(1,2-ethanediyl)-bis-isothiourea (PBITU) reversed the positive effects of exogenous NO. Meanwhile, cPTIO, MB-1, L-NAME, or PBITU alone significantly decreased the vase life, indicating that endogenous NO may play specific roles in cut flower senescence. Exogenous NO decreased 1-aminocyclopro-pane-1-carboxylate oxidase (ACO) activity and ethylene production, and cPTIO was able to prevent the negative effects of NO. This implies that NO may act as an antagonist to ethylene in the senescence of cut rose flowers. Ethylene inhibitors 1-methylcyclopropene (1-MCP) improved vase life and maximum flower diameter, but the promotive effects of 1-MCP could be partially reversed by cPTIO, MB-1, or L-NAME, suggesting that endogenous NO in cut rose flowers may play a crucial role in the cut rose flowers senescence regulated by ethylene. Additionally, 1-MCP treatments increased NOS activity and endogenous NO production, while depressing ACO activity and ethylene production in cut rose. Thus, NO might decrease ethylene output by inhibiting ACO activity in cut rose flowers, thereby vase life being increased. Altogether, the results suggest that NO may function as a signal molecule involved in the senescence of cut rose regulated by ethylene. (C) 2013 Elsevier B.V. All rights reserved.