Cadmium‐mediated toxicity in plant cells is associated with the DCD / NRP ‐mediated cell death response

2021 ◽  
Author(s):  
Iana Pedro Silva Quadros ◽  
Nayara Nolasco Madeira ◽  
Virgílio Adriano Pereira Loriato ◽  
Thaina Fernanda Fillietaz Saia ◽  
Jéssica Coutinho Silva ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cells ◽  
Cell Death Response

scholarly journals The bacterial type III-secreted protein AvrRps4 is a bipartite effector

2017 ◽  
Author(s):  
◽  
Morgan K. Halane
Keyword(s):  
Cell Death ◽  
Immune System ◽  
Resistance Genes ◽  
Pathogenic Bacteria ◽  
Global Climate ◽  
Plant Cells ◽  
Effector Proteins ◽  
Effector Domain ◽  
Cell Death Response ◽  
The Face

Like humans, plants have an immune system to protect themselves against invading pathogens. Unlike humans, however, the plant immune system is inborn and genetically predetermined by resistance genes. Pathogenic bacteria secrete proteins (effectors) into plant cells which manipulate the host cell, often to the benefit of the pathogen. The proteins encoded by resistance genes in resistant plants can specifically detect these effectors and ramp up a potent immune response, often resulting in cell death. By studying these effector proteins and how hosts can recognize them we hope to generate novel, durable methods to protect economically important plants from devastating pathogens. With a rapidly growing population in the face of global climate change it is more important than ever to protect the plants which we all use for food, fiber, and fuel. The effector AvrRps4 is recognized by the protein pair RPS4/RRS1. After delivery into plant cells AvrRps4 is processed into two parts (AvrRps4N and AvrRps4C). AvrRps4C was shown to trigger a cell death response in turnip and has been the most well-studied domain of AvrRps4. My research shows that AvrRps4N is also a functional effector domain. In some plants, in the absence of AvrRps4C, it enhances bacterial virulence. In resistant plants it enhances immunity in the presence of AvrRps4C. Finally, I show that AvrRps4N alone can trigger cell death on some plants, further confirming its role as a bona fide effector domain.

Characterization of cell death process in plant cells induced by hipoxia and anoxia

2000 ◽  
Vol 28 (5) ◽  
pp. A372-A372
Author(s):  
E. N. Baranova ◽  
N. V. Kononenko ◽  
T. V. Bragina ◽  
G. M. Grineva ◽  
T. P. Astafurova ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cells ◽  
Death Process ◽  
Cell Death Process

scholarly journals Antifungal and Anti-Biofilm Effects of Caffeic Acid Phenethyl Ester on Different Candida Species

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1359
Author(s):  
Ibrahim Alfarrayeh ◽  
Edit Pollák ◽  
Árpád Czéh ◽  
András Vida ◽  
Sourav Das ◽  
...  
Keyword(s):  
Cell Death ◽  
Candida Species ◽  
Caffeic Acid Phenethyl Ester ◽  
Dependent Manner ◽  
Cell Shrinkage ◽  
Nuclear Condensation ◽  
Cell Death Response ◽  
Dose Dependent ◽  
Dose Dependent Effect ◽  
Strain Dependent

This study investigated the effect of CAPE on planktonic growth, biofilm-forming abilities, mature biofilms, and cell death of C. albicans, C. tropicalis, C. glabrata, and C. parapsilosis strains. Our results showed a strain- and dose-dependent effect of CAPE on Candida, and the MIC values were between 12.5 and 100 µg/mL. Similarly, the MBIC values of CAPE ranging between 50 and 100 µg/mL highlighted the inhibition of the biofilm-forming abilities in a dose-dependent manner, as well. However, CAPE showed a weak to moderate biofilm eradication ability (19-49%) on different Candida strains mature biofilms. Both caspase-dependent and caspase-independent apoptosis after CAPE treatment were observed in certain tested Candida strains. Our study has displayed typical apoptotic hallmarks of CAPE-induced chromatin margination, nuclear blebs, nuclear condensation, plasma membrane detachment, enlarged lysosomes, cytoplasm fragmentation, cell wall distortion, whole-cell shrinkage, and necrosis. In conclusion, CAPE has a concentration and strain-dependent inhibitory activity on viability, biofilm formation ability, and cell death response in the different Candida species.

scholarly journals Estradiol-inducible AvrRps4 expression reveals distinct properties of TIR-NLR-mediated effector-triggered immunity

2020 ◽  
Vol 71 (6) ◽  
pp. 2186-2197 ◽  
Author(s):  
Bruno Pok Man Ngou ◽  
Hee-Kyung Ahn ◽  
Pingtao Ding ◽  
Amey Redkar ◽  
Hannah Brown ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Surface Receptor ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Defence Genes ◽  
Surface Receptor ◽  
Effector Triggered Immunity ◽  
Bacterial Effectors

Abstract Plant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of the effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates up-regulation of defence genes, and therefore resistance against bacteria.

scholarly journals A chemical screen for suppressors of the avrRpm1-RPM1-dependent hypersensitive cell death response in Arabidopsis thaliana

Planta ◽  
2010 ◽  
Vol 231 (5) ◽  
pp. 1013-1023 ◽  
Author(s):  
Mario Serrano ◽  
David A. Hubert ◽  
Jeffery L. Dangl ◽  
Paul Schulze-Lefert ◽  
Erich Kombrink
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Chemical Screen
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