Glutathione and Phytochelatins Mediated Redox Homeostasis and Stress Signal Transduction in Plants

2016 ◽  
pp. 285-310 ◽  
Author(s):  
Shweta Singh ◽  
Durgesh Kumar Tripathi ◽  
Devendra Kumar Chauhan ◽  
Nawal Kishore Dubey
Keyword(s):  
Signal Transduction ◽  
Redox Homeostasis ◽  
Stress Signal

scholarly journals Roles of Glutathione in Mediating Abscisic Acid Signaling and Its Regulation of Seed Dormancy and Drought Tolerance

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1620
Author(s):  
Murali Krishna Koramutla ◽  
Manisha Negi ◽  
Belay T. Ayele
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Seed Dormancy ◽  
Growth And Development ◽  
Current Knowledge ◽  
Stomatal Closure ◽  
Redox Homeostasis ◽  
Critical Role ◽  
Stress Conditions ◽  
Signal Perception

Plant growth and development and interactions with the environment are regulated by phytohormones and other signaling molecules. During their evolution, plants have developed strategies for efficient signal perception and for the activation of signal transduction cascades to maintain proper growth and development, in particular under adverse environmental conditions. Abscisic acid (ABA) is one of the phytohormones known to regulate plant developmental events and tolerance to environmental stresses. The role of ABA is mediated by both its accumulated level, which is regulated by its biosynthesis and catabolism, and signaling, all of which are influenced by complex regulatory mechanisms. Under stress conditions, plants employ enzymatic and non-enzymatic antioxidant strategies to scavenge excess reactive oxygen species (ROS) and mitigate the negative effects of oxidative stress. Glutathione (GSH) is one of the main antioxidant molecules playing a critical role in plant survival under stress conditions through the detoxification of excess ROS, maintaining cellular redox homeostasis and regulating protein functions. GSH has recently emerged as an important signaling molecule regulating ABA signal transduction and associated developmental events, and response to stressors. This review highlights the current knowledge on the interplay between ABA and GSH in regulating seed dormancy, germination, stomatal closure and tolerance to drought.

scholarly journals Molecular genetic analysis of cold–regulated gene transcription

2002 ◽  
Vol 357 (1423) ◽  
pp. 877-886 ◽  
Author(s):  
C. Viswanathan ◽  
Jian-Kang Zhu
Keyword(s):  
Signal Transduction ◽  
Genetic Analysis ◽  
Cold Stress ◽  
Gene Transcription ◽  
Cold Hardiness ◽  
Negative Regulator ◽  
Clear Understanding ◽  
Stress Signal ◽  
Responsive Gene ◽  
Responsive Element

Chilling and freezing temperatures adversely affect the productivity and quality of crops. Hence improving the cold hardiness of crop plants is an important goal in agriculture, which demands a clear understanding of cold stress signal perception and transduction. Pharmacological and biochemical evidence shows that membrane rigidification followed by cytoskeleton rearrangement, Ca 2+ influx and Ca 2+ –dependent phosphorylation are involved in cold stress signal transduction. Cold–responsive genes are regulated through C–repeat/dehydration–responsive elements (CRT/DRE) and abscisic acid (ABA)–responsive element cis elements by transacting factors C–repeat binding factors/dehydration–responsive element binding proteins (CBFs/DREBs) and basic leucine zippers (bZIPs) (SGBF1), respectively. We have carried out a forward genetic analysis using chemically mutagenized Arabidopsis plants expressing cold–responsive RD29A promoter–driven luciferase to dissect cold signal transduction. We have isolated the fiery1 ( fry1 ) mutant and cloned the FRY1 gene, which encodes an inositol polyphosphate 1–phosphatase. The fry1 plants showed enhanced induction of stress genes in response to cold, ABA, salt and dehydration due to higher accumulation of the second messenger, inositol (1,4,5)– triphosphate (IP 3 ). Thus our study provides genetic evidence suggesting that cold signal is transduced through changes in IP 3 levels. We have also identified the hos1 mutation, which showed super induction of cold–responsive genes and their transcriptional activators. Molecular cloning and characterization revealed that HOS1 encodes a ring finger protein, which has been implicated as an E3 ubiquitin conjugating enzyme. HOS1 is present in the cytoplasm at normal growth temperatures but accumulates in the nucleus upon cold stress. HOS1 appears to regulate temperature sensing by the cell as cold–responsive gene expression occurs in the hos1 mutant at relatively warm temperatures. Thus HOS1 is a negative regulator, which may be functionally linked to cellular thermosensors to modulate cold–responsive gene transcription.

scholarly journals Functional analysis of the ABA-responsive protein family in ABA and stress signal transduction in Arabidopsis

2013 ◽  
Vol 58 (31) ◽  
pp. 3721-3730 ◽  
Author(s):  
LingYun Liu ◽  
Na Li ◽  
ChunPeng Yao ◽  
SaSa Meng ◽  
ChunPeng Song
Keyword(s):  
Signal Transduction ◽  
Functional Analysis ◽  
Protein Family ◽  
Stress Signal

Abstract 452: Hyperglycemia and Oxidative Stress Impair Fluid Shear Stress-mediated Endothelial Nitric Oxide Synthase Phosphorylation and Activation via Disrupting Adherens Junctions

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Meimei Yin ◽  
Suowen Xu ◽  
Chelsea Wong ◽  
Michael A Mastrangelo ◽  
Zheng-Gen Jin
Keyword(s):  
Oxidative Stress ◽  
Signal Transduction ◽  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Laminar Flow ◽  
Fluid Shear Stress ◽  
Beta Catenin ◽  
Fluid Shear ◽  
Stress Signal ◽  
And Oxidative Stress

Endothelial dysfunction, characterized by a decrease of nitric oxide (NO) bioavailability in the vessel wall, plays a crucial role in the pathogenesis of atherosclerosis. Oxidative stress due to increased reactive oxygen species (ROS) is implicated in endothelial dysfunction associated with diabetes. However the molecular mechanisms by which oxidative stress causes endothelial dysfunction remain incompletely understood. Blood flow, which generates fluid shear stress acting on endothelium, is the most potent physiological stimulus for NO production through endothelial NO synthase (eNOS) activation. Here we report that hyperglycemia and oxidative stress impairs fluid shear stress signal transduction and eNOS activation in endothelium. We found that the exposure of endothelial cells (ECs) to ROS generators such as menadione and xanthine/xanthine oxidase inhibited laminar flow-mediated Akt and eNOS phosphorylation and activation in human endothelial cells. Moreover, ECs pre-exposed to high glucose that generates ROS production in ECs, failed to respond to laminar flow for Akt/eNOS phosphorylation and activation. Consequently NO production from ECs in response to laminar flow was attenuated by high glucose treatment. Mechanistically, we observed that hyperglycemia and oxidative stress altered endothelial adherens junction integrity, manifested by the alternation of the localization of cell-cell junction molecules vascular endothelial cadherin (VE-cadherin) and beta-catenin. Silencing VE-cadherin or beta-catenin with small interference RNA also inhibited laminar flow-mediated signaling for eNOS activation, which mimics the effects of oxidative stress, suggesting that cell-cell junction integrity is critical for fluid shear stress signal transduction and eNOS activation. Collectively, our results demonstrate that hyperglycemia and oxidative stress impair laminar flow-mediated eNOS activation through the alternation of endothelial junction integrity and fluid shear stress signal transduction. Our findings suggest a novel mechanism whereby oxidative stress induces diabetes-associated endothelial dysfunction.

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