Gaupels Frank, Durner Jörg, Kogel Karl-Heinz
Institute of Biochemical Plant Pathology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, D-85764, Germany.
Institute of Phytopathology, Research Center for BioSystems, Land Use and Nutrition, Justus Liebig University Gießen, Gießen, D-35392, Germany.
New Phytol. 2017 Apr;214(2):554-560. doi: 10.1111/nph.14399. Epub 2017 Jan 3.
Rapid long-distance signalling is an emerging topic in plant research, and is particularly associated with responses to biotic and abiotic stress. Systemic acquired resistance (SAR) to pathogen attack is dependent on nitric oxide (NO) and reactive oxygen species (ROS) such as hydrogen peroxide (H O ). By comparison, systemic wound responses (SWRs) and systemic acquired acclimation (SAA) to abiotic stress encounters are triggered by rapid waves of H O , calcium and electrical signalling. Efforts have been made to decipher the relationship between redox messengers, calcium and other known systemic defence signals. Less is known about possible routes of signal transduction throughout the entire plant. Previously, the phloem has been suggested to be a transport conduit for mobile signals inducing SAR, SWR and SAA. This review highlights the role of the phloem in systemic redox signalling by NO and ROS. A not yet identified calcium-dependent NO source and S-nitrosoglutathione reductase are candidate regulators of NO homeostasis in the phloem, whereas ROS concentrations are controlled by NADPH oxidases and the H O -scavenging enzyme ascorbate peroxidase. Possible amplification mechanisms in phloem-mediated systemic redox signalling are discussed.
快速长距离信号传导是植物研究中一个新兴的课题,尤其与对生物和非生物胁迫的反应相关。对病原体攻击的系统获得性抗性(SAR)依赖于一氧化氮(NO)和活性氧(ROS),如过氧化氢(H₂O₂)。相比之下,对非生物胁迫的系统伤口反应(SWRs)和系统获得性驯化(SAA)是由H₂O₂、钙和电信号的快速波动触发的。人们已努力去解读氧化还原信使、钙和其他已知的系统防御信号之间的关系。对于信号在整个植物中的可能转导途径了解较少。此前,韧皮部被认为是诱导SAR、SWR和SAA的移动信号的运输管道。本综述强调了韧皮部在由NO和ROS介导的系统氧化还原信号传导中的作用。一种尚未确定的钙依赖性NO源和S-亚硝基谷胱甘肽还原酶是韧皮部中NO稳态的候选调节因子,而ROS浓度则由NADPH氧化酶和H₂O₂清除酶抗坏血酸过氧化物酶控制。文中讨论了韧皮部介导的系统氧化还原信号传导中可能的放大机制。