scholarly journals The cell wall is crucial for cellular sensitivity to low pH: the role of class III peroxidases and ethylene in cell death in Arabidopsis thaliana roots

2018 ◽  
Author(s):  
Jonathas Pereira das Graças
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Cell Wall ◽  
Low Ph ◽  
Class Iii ◽  
Cellular Sensitivity ◽  
Class Iii Peroxidases

scholarly journals The Class III Peroxidase Encoding Gene AtPrx62 Positively and Spatiotemporally Regulates the Low pH-Induced Cell Death in Arabidopsis thaliana Roots

2020 ◽  
Vol 21 (19) ◽  
pp. 7191
Author(s):  
Jonathas Pereira Graças ◽  
Philippe Ranocha ◽  
Victor Alexandre Vitorello ◽  
Bruno Savelli ◽  
Elisabeth Jamet ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Temporal Correlation ◽  
Low Ph ◽  
Class Iii ◽  
Wild Type ◽  
Knockout Mutant ◽  
Root Cells ◽  
Ph Stress ◽  
Class Iii Peroxidase

Exogenous low pH stress causes cell death in root cells, limiting root development, and agricultural production. Different lines of evidence suggested a relationship with cell wall (CW) remodeling players. We investigated whether class III peroxidase (CIII Prx) total activity, CIII Prx candidate gene expression, and reactive oxygen species (ROS) could modify CW structure during low pH-induced cell death in Arabidopsis thaliana roots. Wild-type roots displayed a good spatio-temporal correlation between the low pH-induced cell death and total CIII Prx activity in the early elongation (EZs), transition (TZs), and meristematic (MZs) zones. In situ mRNA hybridization showed that AtPrx62 transcripts accumulated only in roots treated at pH 4.6 in the same zones where cell death was induced. Furthermore, roots of the atprx62-1 knockout mutant showed decreased cell mortality under low pH compared to wild-type roots. Among the ROS, there was a drastic decrease in O2●− levels in the MZs of wild-type and atprx62-1 roots upon low pH stress. Together, our data demonstrate that AtPrx62 expression is induced by low pH and that the produced protein could positively regulate cell death. Whether the decrease in O2●− level is related to cell death induced upon low pH treatment remains to be elucidated.

Root growth restraint can be an acclimatory response to low pH and is associated with reduced cell mortality: a possible role of class III peroxidases and NADPH oxidases

Plant Biology ◽  
2016 ◽  
Vol 18 (4) ◽  
pp. 658-668 ◽  
Author(s):  
J. P. Graças ◽  
R. Ruiz-Romero ◽  
L. D. Figueiredo ◽  
L. Mattiello ◽  
L. E. P. Peres ◽  
...  
Keyword(s):  
Root Growth ◽  
Low Ph ◽  
Class Iii ◽  
Nadph Oxidases ◽  
Cell Mortality ◽  
Acclimatory Response ◽  
Class Iii Peroxidases

Mixed-ligand copper(ii) Schiff base complexes: the vital role of co-ligands in DNA/protein interactions and cytotoxicity

2017 ◽  
Vol 41 (3) ◽  
pp. 1267-1283 ◽  
Author(s):  
Sellamuthu Kathiresan ◽  
Subramanian Mugesh ◽  
Jamespandi Annaraj ◽  
Maruthamuthu Murugan
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Schiff Base ◽  
Protein Interactions ◽  
Apoptotic Cell ◽  
Vital Role ◽  
Mixed Ligand ◽  
Schiff Base Complexes ◽  
Antibacterial Mechanism

Four new mixed-ligand copper(ii) complexes display an antibacterial mechanism of cell death via cell-wall rupture and cytotoxicity via apoptotic cell death.

scholarly journals Depletion of adipocyte Becn1 leads to lipodystrophy and metabolic dysregulation

2020 ◽  
Author(s):  
Ada Admin ◽  
Young Jin ◽  
Yul Ji ◽  
Yaechan Song ◽  
Sung Sik Choe ◽  
...  
Keyword(s):  
Cell Death ◽  
Adipose Tissue ◽  
Er Stress ◽  
Metabolic Diseases ◽  
Class Iii ◽  
Phosphatidylinositol 3 Kinase ◽  
Metabolic Dysregulation ◽  
A Cell ◽  
Stress Gene

<i>Becn1</i>/Beclin-1<i> </i>is a core component of the class III phosphatidylinositol 3-kinase required for autophagosome formation and vesicular trafficking. Although <i>Becn1</i> has been implicated in numerous diseases such as cancer, aging, and neurodegenerative disease, the role of <i>Becn1</i> in white adipose tissue and related metabolic diseases remains elusive. Here we show that adipocyte-specific <i>Becn1</i> knockout mice develop severe lipodystrophy, leading to adipose tissue inflammation, hepatic steatosis, insulin resistance. Ablation of <i>Becn1</i> in adipocytes stimulates programmed cell death in a cell-autonomous manner, accompanied by elevated ER stress gene expression. Furthermore, we observed that <i>Becn1 </i>depletion sensitized mature adipocytes to ER stress, leading to accelerated cell death. Taken together, these data suggest that adipocyte <i>Becn1</i> would serve as a crucial player for adipocyte survival and adipose tissue homeostasis.

scholarly journals Role of Class III Peroxidases in Stem Lignification of Zinnia elegans Jacq.

2020 ◽  
Author(s):  
Anastasia Tugbaeva ◽  
Alexander Ermoshin ◽  
Dmitriy Plotnikov ◽  
Hada Wuriyanghan ◽  
Irina Kiseleva
Keyword(s):  
Zinnia Elegans ◽  
Class Iii ◽  
Class Iii Peroxidases

scholarly journals Depletion of adipocyte Becn1 leads to lipodystrophy and metabolic dysregulation

2020 ◽  
Author(s):  
Ada Admin ◽  
Young Jin ◽  
Yul Ji ◽  
Yaechan Song ◽  
Sung Sik Choe ◽  
...  
Keyword(s):  
Cell Death ◽  
Adipose Tissue ◽  
Er Stress ◽  
Metabolic Diseases ◽  
Class Iii ◽  
Phosphatidylinositol 3 Kinase ◽  
Metabolic Dysregulation ◽  
A Cell ◽  
Stress Gene

<i>Becn1</i>/Beclin-1<i> </i>is a core component of the class III phosphatidylinositol 3-kinase required for autophagosome formation and vesicular trafficking. Although <i>Becn1</i> has been implicated in numerous diseases such as cancer, aging, and neurodegenerative disease, the role of <i>Becn1</i> in white adipose tissue and related metabolic diseases remains elusive. Here we show that adipocyte-specific <i>Becn1</i> knockout mice develop severe lipodystrophy, leading to adipose tissue inflammation, hepatic steatosis, insulin resistance. Ablation of <i>Becn1</i> in adipocytes stimulates programmed cell death in a cell-autonomous manner, accompanied by elevated ER stress gene expression. Furthermore, we observed that <i>Becn1 </i>depletion sensitized mature adipocytes to ER stress, leading to accelerated cell death. Taken together, these data suggest that adipocyte <i>Becn1</i> would serve as a crucial player for adipocyte survival and adipose tissue homeostasis.

scholarly journals CsPrx25, a class III peroxidase in Citrus sinensis, confers resistance to citrus bacterial canker through the maintenance of ROS homeostasis and cell wall lignification

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Qiang Li ◽  
Xiujuan Qin ◽  
Jingjing Qi ◽  
Wanfu Dou ◽  
Christophe Dunand ◽  
...  
Keyword(s):  
Cell Wall ◽  
Susceptible Variety ◽  
Resistant Variety ◽  
Bacterial Canker ◽  
Class Iii ◽  
Ros Homeostasis ◽  
Citrus Production ◽  
Citrus Bacterial Canker ◽  
Apoplastic Barrier

AbstractCitrus bacterial canker (CBC) results from Xanthomonas citri subsp. citri (Xcc) infection and poses a grave threat to citrus production. Class III peroxidases (CIII Prxs) are key proteins to the environmental adaptation of citrus plants to a range of exogenous pathogens, but the role of CIII Prxs during plant resistance to CBC is poorly defined. Herein, we explored the role of CsPrx25 and its contribution to plant defenses in molecular detail. Based on the expression analysis, CsPrx25 was identified as an apoplast-localized protein that is differentially regulated by Xcc infection, salicylic acid, and methyl jasmone acid in the CBC-susceptible variety Wanjincheng (C. sinensis) and the CBC-resistant variety Calamondin (C. madurensis). Transgenic Wanjincheng plants overexpressing CsPrx25 were generated, and these transgenic plants exhibited significantly increased CBC resistance compared with the WT plants. In addition, the CsPrx25-overexpressing plants displayed altered reactive oxygen species (ROS) homeostasis accompanied by enhanced H2O2 levels, which led to stronger hypersensitivity responses during Xcc infection. Moreover, the overexpression of CsPrx25 enhanced lignification as an apoplastic barrier for Xcc infection. Taken together, the results highlight how CsPrx25-mediated ROS homeostasis reconstruction and cell wall lignification can enhance the resistance of sweet orange to CBC.

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