An Insight into the Role of Salicylic Acid and Jasmonic Acid in Salt Stress Tolerance

Author(s):  
M. Iqbal R. Khan ◽  
Shabina Syeed ◽  
Rahat Nazar ◽  
Naser A. Anjum
2011 ◽  
Vol 30 (4) ◽  
pp. 425-435 ◽  
Author(s):  
Tariq Aftab ◽  
M. Masroor A. Khan ◽  
Jaime A. Teixeira da Silva ◽  
Mohd. Idrees ◽  
M. Naeem ◽  
...  

2019 ◽  
Vol 20 (21) ◽  
pp. 5244 ◽  
Author(s):  
Qi Guo ◽  
Liang Zhao ◽  
Xinqi Fan ◽  
Peng Xu ◽  
Zhenzhen Xu ◽  
...  

Cotton is one of the most economically important crops in the world, and it is exposed to various abiotic stresses during its lifecycle, especially salt stress. However, the molecular mechanisms underlying cotton tolerance to salt stress are still not fully understood due to the complex nature of salt response. Therefore, identification of salt stress tolerance-related functional genes will help us understand key components involved in stress response and provide valuable genes for improving salt stress tolerance via genetic engineering in cotton. In the present study, virus-induced gene silencing of GhWRKY5 in cotton showed enhanced salt sensitivity compared to wild-type plants under salt stress. Overexpression of GarWRKY5 in Arabidopsis positively regulated salt tolerance at the stages of seed germination and vegetative growth. Additionally, GarWRKY5-overexpressing plants exhibited higher activities of superoxide dismutase (SOD) and peroxidase (POD) under salt stress. The transcriptome sequencing analysis of transgenic Arabidopsis plants and wild-type plants revealed that there was enriched coexpression of genes involved in reactive oxygen species (ROS) scavenging (including glutamine S-transferases (GSTs) and SODs) and altered response to jasmonic acid and salicylic acid in the GarWRKY5-OE lines. GarWRKY5 is involved in salt stress response by the jasmonic acid- or salicylic acid-mediated signaling pathway based on overexpression of GarWRKY5 in Arabidopsis and virus-induced gene silencing of GarWRKY5 in cotton.


PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0200566 ◽  
Author(s):  
Chantal Ebel ◽  
Asma BenFeki ◽  
Moez Hanin ◽  
Roberto Solano ◽  
Andrea Chini

2021 ◽  
Vol 54 (2) ◽  
Author(s):  
Zeeshan Rehman ◽  
Abrar Hussain ◽  
Shanzay Saleem ◽  
Sheza Ayaz Khilji ◽  
Zahoor Ahmad Sajid

2000 ◽  
Vol 20 (24) ◽  
pp. 9262-9270 ◽  
Author(s):  
Jun Imai ◽  
Ichiro Yahara

ABSTRACT The role of HSP90 in stress tolerance was investigated inSaccharomyces cerevisiae. Cells showing 20-fold overexpression of Hsc82, an HSP90 homologue in yeast, were hypersensitive to high-NaCl or H-LiCl stresses. Hsc82-overexpressing cells appeared similar to calcineurin-defective cells in salt sensitivity and showed reduced levels of calcineurin-dependent gene expression. Co-overexpression of Cna2, the catalytic subunit of calcineurin, suppressed the hypersensitivity. Cna2 and Hsc82 coimmunoprecipitated from control cells grown under normal conditions but not from stressed cells. In contrast, coimmunoprecipitation was detected with Hsc82-overexpressing cells even after exposure to stresses. Cna2 immune complexes from stressed control cells showed a significant level of calcineurin activity, whereas those from stressed Hsc82-overexpressing cells did not. Treatment of extracts from Hsc82-overexpressing cells with Ca2+-calmodulin increased the calcineurin activity associated with Cna2 immune complexes. Geldanamycin, an inhibitor of HSP90 abolished the coimmunoprecipitation but did not activate calcineurin. When the expression level of Hsc82 decreased to below 30% of the normal level, cells also became hypersensitive to salt stress. In these cells, the amount of Cna2 was reduced, likely as a result of degradation. The present results showed that Hsc82 binds to and stabilizes Cna2 and that dissociation of Cna2 from Hsc82 is necessary for its activation.


2020 ◽  
Vol 42 (3) ◽  
Author(s):  
Qurban Ali ◽  
Muzammal Mateen Azhar ◽  
Arif Malik ◽  
Shahbaz Ahmad ◽  
Muhammad Zafar Saleem ◽  
...  

2020 ◽  
Vol 64 ◽  
pp. 150-158
Author(s):  
L.-L. YU ◽  
Y. LIU ◽  
F. ZHU ◽  
X.-X. GENG ◽  
Y. YANG ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Ru-Feng Song ◽  
Ting-Ting Li ◽  
Wen-Cheng Liu

High salinity causes ionic, osmotic, and oxidative stresses to plants, and the antioxidant enzyme Catalase2 (CAT2) plays a vital role in this process, while how CAT2 expression is regulated during plant response to high salinity remains elusive. Here, we report that phytohormone jasmonic acid (JA) impairs plant salt stress tolerance by repressing CAT2 expression in an MYC2-dependent manner. Exogenous JA application decreased plant salt stress tolerance while the jar1 mutant with reduced bioactive JA-Ile accumulation showed enhanced salt stress tolerance. JA enhanced salt-induced hydrogen peroxide (H2O2) accumulation, while treatment with H2O2-scavenger glutathione compromised such effects of JA on plant H2O2 accumulation and salt stress tolerance. In addition, JA repressed CAT2 expression in salt-stressed wild-type plant but not in myc2, a mutant of the master transcriptional factor MYC2 in JA signaling, therefore, the myc2 mutant exhibited increased salt stress tolerance. Further study showed that mutation of CAT2 largely reverted lower reactive oxygen species (ROS) accumulation, higher CAT activity, and enhanced salt stress tolerance of the myc2 mutant in myc2 cat2-1 double mutant, revealing that CAT2 functions downstream JA-MYC2 module in plant response to high salinity. Together, our study reveals that JA impairs Arabidopsis seedling salt stress tolerance through MYC2-mediated repression of CAT2 expression.


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