Nitric oxide as a secondary messenger during stomatal closure as a part of plant immunity response against pathogens

被引:40
|
作者
Agurla, Srinivas [1 ]
Gayatri, Gunja [1 ]
Raghavendra, Agepati S. [1 ]
机构
[1] Univ Hyderabad, Sch Life Sci, Dept Plant Sci, Hyderabad 500046, Andhra Pradesh, India
来源
NITRIC OXIDE-BIOLOGY AND CHEMISTRY | 2014年 / 43卷
关键词
Defense response in plants; Nitric oxide; Nitrosylation; Reactive oxygen species; Stomatal closure; PHOSPHATIDIC-ACID PRODUCTION; INDUCED DEFENSE RESPONSES; ABSCISIC-ACID; REACTIVE OXYGEN; HYDROGEN-SULFIDE; INNATE IMMUNITY; METHYL JASMONATE; S-NITROSYLATION; SALICYLIC-ACID; CYTOSOLIC ALKALINIZATION;
D O I
10.1016/j.niox.2014.07.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Stomata facilitate the loss of water, as well as CO2 uptake for photosynthesis. In addition, stomatal closure restricts the entry of pathogens into leaves and forms a part of plant defense response. Plants have evolved ways to modulate stomata by plant hormones as well as microbial elicitors, including pathogen/microbe associated molecular patterns. Stomatal closure initiated by signals of either abiotic or biotic factors results from the loss of guard cell turgor due mainly to K+/anion efflux. Nitric oxide (NO) is a key element among the signaling elements leading to stomatal closure, hypersensitive response and programmed cell death. Due to the growing importance of NO as signaling molecule in plants, and the strong relation between stomata and pathogen resistance, we attempted to present a critical overview of plant innate immunity, in relation to stomatal closure. The parallel role of NO during plant innate immunity and stomatal closure is highlighted. The cross-talk between NO and other signaling components, such as reactive oxygen species (ROS) is discussed. The possible sources of NO and mechanisms of NO action, through post-translational modification of proteins are discussed. The mini-review is concluded with remarks on the existing gaps in our knowledge and suggestions for future research. (c) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:89 / 96
页数:8
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