scholarly journals Pattern-Triggered Immunity Suppresses Programmed Cell Death Triggered by Fumonisin B1

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e60769 ◽  
Author(s):  
Daisuke Igarashi ◽  
Gerit Bethke ◽  
Yuan Xu ◽  
Kenichi Tsuda ◽  
Jane Glazebrook ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Fumonisin B1

scholarly journals Ethylene-Responsive AP2/ERF Transcription Factor MACD1 Participates in Phytotoxin-Triggered Programmed Cell Death

2013 ◽  
Vol 26 (8) ◽  
pp. 868-879 ◽  
Author(s):  
Keisuke Mase ◽  
Nobuaki Ishihama ◽  
Hitoshi Mori ◽  
Hideki Takahashi ◽  
Hironori Kaminaka ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Programmed Cell Death ◽  
Fumonisin B1 ◽  
Structural Analog ◽  
Necrotrophic Pathogen ◽  
Factors Affecting ◽  
Downstream Signaling ◽  
Upregulated Genes ◽  
Erf Transcription Factor

To investigate plant programmed cell death (PCD), we developed the model system using phytotoxin AAL, which is produced by necrotrophic pathogen Alternaria alternata f. sp. lycopersici, and AAL-sensitive Nicotiana umbratica. We previously reported that ethylene (ET) signaling plays a pivotal role in AAL-triggered cell death (ACD). However, downstream signaling of ET to ACD remains unclear. Here, we show that the modulator of AAL cell death 1 (MACD1), which is an APETALA2/ET response factor (ERF) transcription factor, participates in ACD and acts downstream of ET signaling during ACD. MACD1 is a transcriptional activator and MACD1 overexpression plants showed earlier ACD induction than control plants, suggesting that MACD1 positively regulates factors affecting cell death. To investigate the role of MACD1 in PCD, we used Arabidopsis thaliana and a structural analog of AAL, fumonisin B1 (FB1). FB1-triggered cell death was compromised in ET signaling and erf102 mutants. The loh2 mutants showed sensitivity to AAL, and the loh2-1/erf102 double mutant compromised ACD, indicating that ERF102 also participates in ACD. To investigate the PCD-associated genes regulated by ERF102, we compared our microarray data using ERF102 overexpression plants with the database of upregulated genes by AAL treatment in loh2 mutants, and found genes under the control of ERF102 in ACD.

scholarly journals Hijacking of the jasmonate pathway by the mycotoxin fumonisin B1 (FB1) to initiate programmed cell death in Arabidopsis is modulated by RGLG3 and RGLG4

2015 ◽  
Vol 66 (9) ◽  
pp. 2709-2721 ◽  
Author(s):  
Xu Zhang ◽  
Qian Wu ◽  
Shao Cui ◽  
Jiao Ren ◽  
Wanqiang Qian ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Fumonisin B1

scholarly journals Classic myrosinase-dependent degradation of indole glucosinolate attenuates fumonisin B1-induced programmed cell death in Arabidopsis

2015 ◽  
Vol 81 (6) ◽  
pp. 920-933 ◽  
Author(s):  
Yanting Zhao ◽  
Jiansheng Wang ◽  
Yuanyuan Liu ◽  
Huiying Miao ◽  
Congxi Cai ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Fumonisin B1 ◽  
Indole Glucosinolate

scholarly journals Ceramide Synthase-dependent Ceramide Generation and Programmed Cell Death

2011 ◽  
Vol 286 (18) ◽  
pp. 15929-15942 ◽  
Author(s):  
Thomas D. Mullen ◽  
Russell W. Jenkins ◽  
Christopher J. Clarke ◽  
Jacek Bielawski ◽  
Yusuf A. Hannun ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
De Novo ◽  
Fumonisin B1 ◽  
Membrane Permeabilization ◽  
Ceramide Synthase ◽  
Plasma Membrane Permeabilization ◽  
Ceramide Generation ◽  
Uv C

The sphingolipid ceramide has been widely implicated in the regulation of programmed cell death or apoptosis. The accumulation of ceramide has been demonstrated in a wide variety of experimental models of apoptosis and in response to a myriad of stimuli and cellular stresses. However, the detailed mechanisms of its generation and regulatory role during apoptosis are poorly understood. We sought to determine the regulation and roles of ceramide production in a model of ultraviolet light-C (UV-C)-induced programmed cell death. We found that UV-C irradiation induces the accumulation of multiple sphingolipid species including ceramide, dihydroceramide, sphingomyelin, and hexosylceramide. Late ceramide generation was also found to be regulated by Bcl-xL, Bak, and caspases. Surprisingly, inhibition of de novo synthesis using myriocin or fumonisin B1 resulted in decreased overall cellular ceramide levels basally and in response to UV-C, but only fumonisin B1 inhibited cell death, suggesting the presence of a ceramide synthase (CerS)-dependent, sphingosine-derived pool of ceramide in regulating programmed cell death. We found that this pool did not regulate the mitochondrial pathway, but it did partially regulate activation of caspase-7 and, more importantly, was necessary for late plasma membrane permeabilization. Attempting to identify the CerS responsible for this effect, we found that combined knockdown of CerS5 and CerS6 was able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. These data identify a novel role for CerS and the sphingosine salvage pathway in regulating membrane permeability in the execution phase of programmed cell death.

Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors

2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  
Keyword(s):  
Cell Death ◽  
Venous Thromboembolism ◽  
Programmed Cell Death ◽  
Brain Tumors ◽  
Primary Brain Tumors

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

Dynamical analysis of the programmed cell death pathway

2007 ◽  
Author(s):  
Luciano Carotenuto ◽  
Vincenza Pace ◽  
Dina Bellizzi ◽  
Giovanna De Benedictis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dynamical Analysis ◽  
Cell Death Pathway

Biological response of the organism to the introduction of metal nanocomposites

2020 ◽  
pp. 761-762
Author(s):  
L. M. Sosedova ◽  
V. S. Rukavishnikov ◽  
E. A. Titov
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Biological Response ◽  
Brain Cell ◽  
Metal Nanocomposites ◽  
The Brain

The results of a study on rats toxicity of nanoparticles of metals bismuth, gadolinium and silver encapsulated in a natural biopolymer matrix arabinogalactan are presented. When intake of nanocomposite of silver revealed the readiness of the brain cell to apoptosis. The effect of bismuth and gadolinium nanocomposites did not cause an increase in the process of programmed cell death.

Sign in / Sign up

Export Citation Format

Share Document