scholarly journals Physio-ultrastructural footprints and iTRAQ-based proteomic approach unravel the role of Piriformospora indica-colonization in counteracting cadmium toxicity in rice

2021 ◽  
Vol 220 ◽  
pp. 112390
Author(s):  
Tichaona Sagonda ◽  
Muhammad Faheem Adil ◽  
Shafaque Sehar ◽  
Adeela Rasheed ◽  
Heren Issaka Joan ◽  
...  
2014 ◽  
Vol 60 (3) ◽  
pp. 121-131 ◽  
Author(s):  
Surasak Siripornadulsil ◽  
Lalita Thanwisai ◽  
Wilailak Siripornadulsil

Cupriavidus taiwanensis KKU2500-3 is a cadmium (Cd)-tolerant bacterial strain that was previously isolated from rice fields contaminated with high levels of Cd. In 500 μmol/L CdCl2, the KKU2500-3 strain grew slower and with a more prolonged lag-phase than when grown in the absence of Cd. A proteomic approach was used to characterize the protein expression in the Cd-tolerant bacteria C. taiwanensis KKU2500-3 during growth under Cd stress. When compared with the untreated cells, a total of 982 differentially expressed protein spots were observed in the CdCl2-treated cells, and 59 and 10 spots exhibited >2- and >4-fold changes, respectively. The level of up- and downregulation varied from 2.01- to 11.26-fold and from 2.01- to 5.34-fold, respectively. Of the 33 differentially expressed protein spots analyzed by MALDI TOF MS/MS, 19 spots were successfully identified, many of which were involved in stress responses. The most highly upregulated protein (+7.95-fold) identified was the chaperone GroEL, which indicated that this factor likely contributed to the bacterial survival and growth in response to Cd toxicity. Detection of the downregulated protein flagellin (–3.52-fold) was consistent with the less effective ATP-mediated and flagella-driven motility. The flagella-losing cells were also observed in the Cd-treated bacteria when analyzed by scanning electron microscopy. Thus, the Cd-stressed cells may downregulate pathways involving ATP utilization in favor of other mechanisms in response to Cd toxicity. When the KKU2500-3 strain was grown in the presence of Cd, H2S was not detected, suggesting a possible role of the sulfur in precipitation with Cd. Apart from a general response, no specific process could be determined using the present proteomic approach. However, the potential role of protein folding-mediated GroEL, flagella-mediated motility and CdS biotransformation in Cd toxicity response observed in this study as well as the extent of Cd-tolerant mechanisms using other methods could facilitate the future application of this strain in addressing Cd environmental contamination.


Author(s):  
Linru Huang ◽  
Zhijia Fang ◽  
Jian Gao ◽  
Jingwen Wang ◽  
Yongbin Li ◽  
...  

1991 ◽  
Vol 10 ◽  
pp. 23
Author(s):  
A.L. Buchman ◽  
A. Moukarzel ◽  
M.E. Ament
Keyword(s):  

Eisei kagaku ◽  
1986 ◽  
Vol 32 (2) ◽  
pp. 109-113
Author(s):  
SATOMI ONOSAKA ◽  
KYONGSON MIN ◽  
CHIKAKO FUKUHARA ◽  
KEIICHI TANAKA
Keyword(s):  

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Jochen Steppan ◽  
Ivy Wang ◽  
Yehudit Bergman ◽  
Siqi Tan ◽  
Sandeep Jandu ◽  
...  

Introduction: Stiffening of the central vasculature is a strong and independent predictor of adverse cardiovascular events. Vascular stiffening is a complex process that involves changes in the vessel wall composition and smooth muscle cell (SMC) function. We recently used an unbiased proteomic approach to identify Lysyl oxidase like 2 (LOXL2) as a potential new target in vascular stiffness. The goal of this study is to characterize the role of LOXL2 in vascular stiffening and its potential as a target to reverse vascular stiffness associated with hypertension. Results: We demonstrate that decreased nitric oxide (NO) bioavailability results in increased secretion and activity of LOXL2 in SMCs. LOXL2 knockdown markedly attenuates SMC adhesion, motility, and proliferation and results in diminished matrix deposition. LOXL2 knockdown also results in striking changes in the stiffness and cytoskeletal remodeling events in CMSs. Tensile testing shows that intact aortas of LOXL2+/- animals are stiffer when compared with those from wild type mice, while there is no difference in decellularized vessels. We next investigated the role of LOXL2 in the development of hypertension using angiotensin II (AngII) infusion in LOXL2+/- (group 1) and wild type (WT; group 2) mice. BP and pulse wave velocity (PWV) increased significantly with AngII infusion in both groups during the study period, without a significant change in heart rate. Compared to WT animals, contractile responsiveness was markedly diminished in LOXL2+/- animals at baseline as well as with AngII infusion when compared with untreated controls. The NO- dependent vasodilatory response to acetylcholine was identical at baseline and diminished significantly with AngII infusion in both groups of animals. There was no difference between the groups in the endothelium-independent response to sodium nitroprusside. Conclusion: In this study, we demonstrated the role of NO in the regulation of LOXL2. Interestingly, LOXL2 appears to have a dual role in vascular stiffness by affecting both SMC function as well as matrix composition. We therefore conclude that LOXL2 is a novel target involved in vascular stiffness that requires further characterization to elicit the possibility of therapeutic intervention.


2009 ◽  
Vol 57 (3) ◽  
pp. 321-333 ◽  
Author(s):  
H. Moussa ◽  
S. EL-Gamal

Treatment with CdCl 2 (0, 100, 400 and 1000 μM) resulted in the inhibition of root dry biomass and root elongation and to increased Cd accumulation in the roots. These treatments also decreased the relative water content, chlorophyll content, 14 CO fixation, phosphoenol pyruvate carboxylase and ribulose-1,5-bisphosphate carboxylase activity and abscisic acid (ABA) content, while increasing the malondialdehyde, hydrogen peroxide and free proline contents and causing changes in the chloroplast and root ultrastructure. Pretreatment of seeds with SA (500 μM) for 20 h resulted in the amelioration of these effects.


2005 ◽  
Vol 17 (1) ◽  
pp. 21-34 ◽  
Author(s):  
María P. Benavides ◽  
Susana M. Gallego ◽  
María L. Tomaro

Heavy metals are important environmental pollutants and their toxicity is a problem of increasing significance for ecological, evolutionary, nutritional, and environmental reasons. Plants posses homeostatic cellular mechanisms to regulate the concentration of metal ions inside the cell to minimize the potential damage that could result from the exposure to nonessential metal ions. This paper summarizes present knowledge in the field of higher plant responses to cadmium, an important environmental pollutant. Knowledge concerning metal toxicity, including mechanisms of cadmium homeostasis, uptake, transport and accumulation are evaluated. The role of the cell wall, the plasma membrane and the mycorrhizas, as the main barriers against cadmium entrance to the cell, as well as some aspects related to phytochelatin-based sequestration and compartmentalization processes are also reviewed. Cadmium-induced oxidative stress was also considered as one of the most studied topics of cadmium toxicity.


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