SPL5, a cell death and defense-related gene, encodes a putative splicing factor 3b subunit 3 (SF3b3) in rice

2011 ◽  
Vol 30 (2) ◽  
pp. 939-949 ◽  
Author(s):  
Xifeng Chen ◽  
Liang Hao ◽  
Jianwei Pan ◽  
Xixi Zheng ◽  
Guanghuai Jiang ◽  
...  
Keyword(s):  
Cell Death ◽  
Splicing Factor ◽  
Related Gene ◽  
Defense Related Gene ◽  
A Cell

scholarly journals Pseudomonas fluorescens PTA-CT2 Triggers Local and Systemic Immune Response Against Botrytis cinerea in Grapevine

2015 ◽  
Vol 28 (10) ◽  
pp. 1117-1129 ◽  
Author(s):  
Charlotte Gruau ◽  
Patricia Trotel-Aziz ◽  
Sandra Villaume ◽  
Fanja Rabenoelina ◽  
Christophe Clément ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Pseudomonas Fluorescens ◽  
Botrytis Cinerea ◽  
Defense Responses ◽  
Systemic Resistance ◽  
Related Gene ◽  
Plant Parts ◽  
Defense Related Gene ◽  
Below Ground

Although induced systemic resistance (ISR) is well-documented in the context of plant–beneficial bacteria interactions, knowledge about the local and systemic molecular and biochemical defense responses before or upon pathogen infection in grapevine is very scarce. In this study, we first investigated the capacity of grapevine plants to express immune responses at both above- and below-ground levels upon interaction with a beneficial bacterium, Pseudomonas fluorescens PTA-CT2. We then explored whether the extent of priming state could contribute to the PTA-CT2-induced ISR in Botrytis cinerea–infected leaves. Our data provide evidence that this bacterium colonized grapevine roots but not the above-ground plant parts and altered the plant phenotype that displayed multiple defense responses both locally and systemically. The grapevine roots and leaves exhibited distinct patterns of defense-related gene expression during root colonization by PTA-CT2. Roots responded faster than leaves and some responses were more strongly upregulated in roots than in leaves and vice versa for other genes. These responses appear to be associated with some induction of cell death in roots and a transient expression of HSR, a hypersensitive response-related gene in both local (roots) and systemic (leaves) tissues. However, stilbenic phytoalexin patterns followed opposite trends in roots compared with leaves but no phytoalexin was exuded during plant-bacterium interaction, suggesting that roots could play an important role in the transfer of metabolites contributing to immune response at the systemic level. Unexpectedly, in B. cinerea–infected leaves PTA-CT2-mediated ISR was accompanied in large part by a downregulation of different defense-related genes, including HSR. Only phytoalexins and glutathion-S-transferase 1 transcripts were upregulated, while the expression of anthocyanin biosynthetic genes was maintained at a higher level than the control. This suggests that decreased expression of HSR, as a marker of cell death, and activation of secondary metabolism pathways could be responsible for a reduced B. cinerea colonization capacity in bacterized plants.

A Cell Death Pathway Induced by Antibody-Mediated Cross-Linking of CD45 on Lymphocytes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 421-440 ◽  
Author(s):  
Ann-Muriel Steff ◽  
Marylene Fortin ◽  
Fabianne Philippoussis ◽  
Sylvie Lesage ◽  
Chantal Arguin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Linking ◽  
Cell Death Pathway ◽  
A Cell

scholarly journals Mitochondria and Pharmacologic Cardiac Conditioning—At the Heart of Ischemic Injury

2021 ◽  
Vol 22 (6) ◽  
pp. 3224
Author(s):  
Christopher Lotz ◽  
Johannes Herrmann ◽  
Quirin Notz ◽  
Patrick Meybohm ◽  
Franz Kehl
Keyword(s):  
Cell Death ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Research Field ◽  
Calcium Handling ◽  
Control Mechanisms ◽  
Intrinsic Resistance ◽  
Atp Production ◽  
Cardiac Conditioning ◽  
A Cell

Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.

scholarly journals Hypoxic neuronal necrosis: Protein synthesis-independent activation of a cell death program

2003 ◽  
Vol 100 (5) ◽  
pp. 2825-2830 ◽  
Author(s):  
J. Niquet ◽  
R. A. Baldwin ◽  
S. G. Allen ◽  
D. G. Fujikawa ◽  
C. G. Wasterlain
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Neuronal Necrosis ◽  
Cell Death Program ◽  
A Cell

Overexpression of the TIR-X gene results in a dwarf phenotype and activation of defense-related gene expression in Arabidopsis thaliana

2014 ◽  
Vol 171 (6) ◽  
pp. 382-388 ◽  
Author(s):  
Hiroaki Kato ◽  
Tamao Saito ◽  
Hidetaka Ito ◽  
Yoshibumi Komeda ◽  
Atsushi Kato
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Related Gene ◽  
Dwarf Phenotype ◽  
Defense Related Gene ◽  
X Gene

scholarly journals Identification of Selenoprotein P Fragments as a Cell-Death Inhibitory Factor

2003 ◽  
Vol 26 (6) ◽  
pp. 794-798 ◽  
Author(s):  
Masaki Hirashima ◽  
Takeshi Naruse ◽  
Hiroaki Maeda ◽  
Chikateru Nozaki ◽  
Yoshiro Saito ◽  
...  
Keyword(s):  
Cell Death ◽  
Inhibitory Factor ◽  
Selenoprotein P ◽  
A Cell

Increased cell death in osteopontin-deficient cardiac fibroblasts occurs by a caspase-3-independent pathway

2004 ◽  
Vol 287 (4) ◽  
pp. H1730-H1739 ◽  
Author(s):  
Ron Zohar ◽  
Baoqian Zhu ◽  
Peter Liu ◽  
Jaro Sodek ◽  
C. A. McCulloch
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Cardiac Fibroblasts ◽  
Chromatin Condensation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Wild Type ◽  
Nuclear Fragmentation ◽  
A Cell

Reperfusion-induced oxidative injury to the myocardium promotes activation and proliferation of cardiac fibroblasts and repair by scar formation. Osteopontin (OPN) is a proinflammatory cytokine that is upregulated after reperfusion. To determine whether OPN enhances fibroblast survival after exposure to oxidants, cardiac fibroblasts from wild-type (WT) or OPN-null (OPN−/−) mice were treated in vitro with H2O2to model reperfusion injury. Within 1 h, membrane permeability to propidium iodide (PI) was increased from 5 to 60% in OPN−/−cells but was increased to only 20% in WT cells. In contrast, after 1–8 h of treatment with H2O2, the percent of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-stained cells was more than twofold higher in WT than OPN−/−cells. Electron microscopy of WT cells treated with H2O2showed chromatin condensation, nuclear fragmentation, and cytoplasmic and nuclear shrinkage, which are consistent with apoptosis. In contrast, H2O2-treated OPN−/−cardiac fibroblasts exhibited cell and nuclear swelling and membrane disruption that are indicative of cell necrosis. Treatment of OPN−/−and WT cells with a cell-permeable caspase-3 inhibitor reduced the percentage of TUNEL staining by more than fourfold in WT cells but decreased staining in OPN−/−cells by ∼30%. Although the percentage of PI-permeable WT cells was reduced threefold, the percent of PI-permeable OPN−/−cells was not altered. Restoration of OPN expression in OPN−/−fibroblasts reduced the percentage of PI-permeable cells but not TUNEL staining after H2O2treatment. Thus H2O2-induced cell death in OPN-deficient cardiac fibroblasts is mediated by a caspase-3-independent, necrotic pathway. We suggest that the increased expression of OPN in the myocardium after reperfusion may promote fibrosis by protecting cardiac fibroblasts from cell death.

scholarly journals Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain

2015 ◽  
Vol 28 (1) ◽  
pp. 18-31 ◽  
Author(s):  
Jeremy Duncan ◽  
Niping Wang ◽  
Xiao Zhang ◽  
Shakevia Johnson ◽  
Sharonda Harris ◽  
...  
Keyword(s):  
Cell Death ◽  
Rat Brain ◽  
Social Stress ◽  
Chronic Social Stress ◽  
A Cell

The Fas ligand as a cell death factor and signal transducer

2003 ◽  
Vol 3 (12) ◽  
pp. 33-46 ◽  
Author(s):  
Andreas Linkermann ◽  
Jing Qian ◽  
Dieter Kabelitz ◽  
Ottmar Janssen
Keyword(s):  
Cell Death ◽  
Fas Ligand ◽  
Signal Transducer ◽  
A Cell
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