An ERF transcription factor from Tamarix hispida , ThCRF1, can adjust osmotic potential and reactive oxygen species scavenging capability to improve salt tolerance

Plant Science ◽  
2017 ◽  
Vol 265 ◽  
pp. 154-166 ◽  
Author(s):  
Liping Qin ◽  
Liuqiang Wang ◽  
Yong Guo ◽  
Yan Li ◽  
Halik Ümüt ◽  
...  
Forests ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1633
Author(s):  
Li Ren ◽  
Fangrui Li ◽  
Jing Jiang ◽  
Huiyu Li

The plant-specific transcription factors TEOSINTE BRANCHED1/CYCLO IDEA/PROLIFERATING CELL FACTOR1 (TCP) act as developmental regulators that have many roles in the growth and development processes throughout the entire life span of plants. TCP transcription factors are responsive to endogenous and environmental signals, such as salt stress. However, studies on the role of the TCP genes in salt stress response have rarely focused on woody plants, especially forest trees. In this study, the BpTCP3 gene, a CYC/TB1 subfamily member, isolated from Betula platyphylla Sukaczev, was significantly influenced by salt stress. The β-glucuronidase (GUS) staining analysis of transgenic B. platyphylla harboring the BpTCP3 promoter fused to the reporter gene GUS (pBpTCP3::GUS) further confirmed that the BpTCP3 gene acts a positive regulatory position in salt stress. Under salt stress, we found that the BpTCP3 overexpressed lines had increased relative/absolute high growth but decreased salt damage index, hydrogen peroxide (H2O2), and malondialdehyde (MDA) levels versus wild-type (WT) plants. Conversely, the BpTCP3 suppressed lines exhibited sensitivity to salt stress. These results indicate that the BpTCP3 transcription factor improves the salt tolerance of B. platyphylla by reducing reactive oxygen species damage, which provides useful clues for the functions of the CYC/TB1 subfamily gene in the salt stress response of B. platyphylla.


2014 ◽  
Vol 58 (4) ◽  
pp. 751-757 ◽  
Author(s):  
L. H. Xu ◽  
W. Y. Wang ◽  
J. J. Guo ◽  
J. Qin ◽  
D. Q. Shi ◽  
...  

2005 ◽  
Vol 25 (19) ◽  
pp. 8520-8530 ◽  
Author(s):  
Peter Storz ◽  
Heike Döppler ◽  
Alex Toker

ABSTRACT Efficient elimination of mitochondrial reactive oxygen species (mROS) correlates with increased cellular survival and organism life span. Detoxification of mitochondrial ROS is regulated by induction of the nuclear SOD2 gene, which encodes the manganese-dependent superoxide dismutase (MnSOD). However, the mechanisms by which mitochondrial oxidative stress activates cellular signaling pathways leading to induction of nuclear genes are not known. Here we demonstrate that release of mROS activates a signal relay pathway in which the serine/threonine protein kinase D (PKD) activates the NF-κB transcription factor, leading to induction of SOD2. Conversely, the FOXO3a transcription factor is dispensable for mROS-induced SOD2 induction. PKD-mediated MnSOD expression promotes increased survival of cells upon release of mROS, suggesting that mitochondrion-to-nucleus signaling is necessary for efficient detoxification mechanisms and cellular viability.


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