Induction of phosphatidylinositol 3-kinase-mediated endocytosis by salt stress leads to intracellular production of reactive oxygen species and salt tolerance

2007 ◽  
Vol 51 (2) ◽  
pp. 185-197 ◽  
Author(s):  
Yehoram Leshem ◽  
Lior Seri ◽  
Alex Levine
2018 ◽  
Vol 19 (11) ◽  
pp. 3347 ◽  
Author(s):  
Yayun Wang ◽  
Hui Zhao ◽  
Hua Qin ◽  
Zixuan Li ◽  
Hai Liu ◽  
...  

The root plays an important role in the responses of plants to stresses, but the detailed mechanisms of roots in stress responses are still obscure. The GDP-mannose pyrophosphate synthetase (GMPase) OsVTC1-3 is a key factor of ascorbic acid (AsA) synthesis in rice roots. The present study showed that the transcript of OsVTC1-3 was induced by salt stress in roots, but not in leaves. Inhibiting the expression of OsVTC1-3 by RNA interfering (RI) technology significantly impaired the tolerance of rice to salt stress. The roots of OsVTC1-3 RI plants rapidly produced more O2−, and later accumulated amounts of H2O2 under salt stress, indicating the impaired tolerance of OsVTC1-3 RI plants to salt stress due to the decreasing ability of scavenging reactive oxygen species (ROS). Moreover, exogenous AsA restored the salt tolerance of OsVTC1-3 RI plants, indicating that the AsA synthesis in rice roots is an important factor for the response of rice to salt stress. Further studies showed that the salt-induced AsA synthesis was limited in the roots of OsVTC1-3 RI plants. The above results showed that specifically regulating AsA synthesis to scavenge ROS in rice roots was one of important factors in enhancing the tolerance of rice to salt stress.


2007 ◽  
Vol 293 (4) ◽  
pp. L913-L922 ◽  
Author(s):  
Georgia Chachami ◽  
Apostolia Hatziefthimiou ◽  
Panagiotis Liakos ◽  
Maria G. Ioannou ◽  
Georgios K. Koukoulis ◽  
...  

Airway smooth muscle (ASM) cells are characterized by phenotypic plasticity and can switch between differentiated and proliferative phenotypes. In rabbit tracheal ASM cells that had been differentiated in vitro by serum starvation, readdition of FBS caused initiation of proliferation and induction of nuclear and transcriptionally active hypoxia-inducible factor (HIF)-1α. In addition, FBS stimulated the induction of HIF-1α by the hypoxia mimetic cobalt. Treatment with actinomycin D, cycloheximide, the phosphatidylinositol 3-kinase inhibitors LY-294002 and wortmannin or the reactive oxygen species scavenger diphenyleneiodonium inhibited the FBS-dependent induction of HIF-1α. These data indicate that, in differentiated ASM cells, FBS upregulates HIF-1α by a transcription-, translation-, phosphatidylinositol 3-kinase-, and reactive oxygen species-dependent mechanism. Interestingly, addition of FBS and cobalt also induced HIF-1α in organ cultures of rabbit trachea strips and synergistically increased their contractile response to ACh, suggesting that HIF-1α might be implicated in airway hypercontractility.


FEBS Letters ◽  
2005 ◽  
Vol 579 (5) ◽  
pp. 1243-1248 ◽  
Author(s):  
Jung Hee Joo ◽  
Ho Jung Yoo ◽  
Inhwan Hwang ◽  
June Seung Lee ◽  
Kyoung Hee Nam ◽  
...  

2007 ◽  
Vol 27 (14) ◽  
pp. 5214-5224 ◽  
Author(s):  
Jianhua Zhu ◽  
Xinmiao Fu ◽  
Yoon Duck Koo ◽  
Jian-Kang Zhu ◽  
Francis E. Jenney ◽  
...  

ABSTRACT The myristoylated calcium sensor SOS3 and its interacting protein kinase, SOS2, play critical regulatory roles in salt tolerance. Mutations in either of these proteins render Arabidopsis thaliana plants hypersensitive to salt stress. We report here the isolation and characterization of a mutant called enh1-1 that enhances the salt sensitivity of sos3-1 and also causes increased salt sensitivity by itself. ENH1 encodes a chloroplast-localized protein with a PDZ domain at the N-terminal region and a rubredoxin domain in the C-terminal part. Rubredoxins are known to be involved in the reduction of superoxide in some anaerobic bacteria. The enh1-1 mutation causes enhanced accumulation of reactive oxygen species (ROS), particularly under salt stress. ROS also accumulate to higher levels in sos2-1 but not in sos3-1 mutants. The enh1-1 mutation does not enhance sos2-1 phenotypes. Also, enh1-1 and sos2-1 mutants, but not sos3-1 mutants, show increased sensitivity to oxidative stress. These results indicate that ENH1 functions in the detoxification of reactive oxygen species resulting from salt stress by participating in a new salt tolerance pathway that may involve SOS2 but not SOS3.


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