Proteomics Analysis of Rice Lesion Mimic Mutant (spl1) Reveals Tightly Localized Probenazole-Induced Protein (PBZ1) in Cells Undergoing Programmed Cell Death

2008 ◽  
Vol 7 (4) ◽  
pp. 1750-1760 ◽  
Author(s):  
Sun Tae Kim ◽  
Sang Gon Kim ◽  
Young Hyun Kang ◽  
Yiming Wang ◽  
Jae-Yean Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteomics Analysis ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant ◽  
In Cells

scholarly journals Uncoupled Expression of Nuclear and Plastid Photosynthesis-Associated Genes Contributes to Cell Death in a Lesion Mimic Mutant

2019 ◽  
Vol 31 (1) ◽  
pp. 210-230 ◽  
Author(s):  
Ruiqing Lv ◽  
Zihao Li ◽  
Mengping Li ◽  
Vivek Dogra ◽  
Shanshan Lv ◽  
...  
Keyword(s):  
Cell Death ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant

Blastocystis hominis : evidence for caspase-3-like activity in cells undergoing programmed cell death

2001 ◽  
Vol 87 (7) ◽  
pp. 559-565 ◽  
Author(s):  
Nasirudeen A. ◽  
Singh M. ◽  
Yap E. ◽  
Tan K.
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Caspase 3 ◽  
Blastocystis Hominis ◽  
In Cells

scholarly journals SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
R. A. O. Yuchun ◽  
J. I. A. O. Ran ◽  
W. A. N. G. Sheng ◽  
W. U. Xianmei ◽  
Y. E. Hanfei ◽  
...  
Keyword(s):  
Cell Death ◽  
Salt Stress ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Defense Responses ◽  
Base Substitution ◽  
Wild Type ◽  
Salt Stress Response ◽  
Lesion Mimic

AbstractLesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.

scholarly journals Golgi anti-apoptotic proteins are evolutionarily conserved ion channels that regulate cell death in plants

2019 ◽  
Author(s):  
Maija Sierla ◽  
David L. Prole ◽  
Nuno Saraiva ◽  
Guia Carrara ◽  
Natalia Dinischiotu ◽  
...  
Keyword(s):  
Cell Death ◽  
Ion Channels ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Lesion Mimic ◽  
Evolutionarily Conserved ◽  
Apoptotic Proteins ◽  
Regulate Cell Death

ABSTRACTProgrammed cell death regulates developmental and stress responses in eukaryotes. Golgi anti-apoptotic proteins (GAAPs) are evolutionarily conserved cell death regulators. Human and viral GAAPs inhibit apoptosis and modulate intracellular Ca2+fluxes, and viral GAAPs form cation-selective channels. Although most mammalian cell death regulators are not conserved at the sequence level in plants, the GAAP gene family shows expansion, with five paralogues (AtGAAP1-5) in the Arabidopsis genome. We pursued molecular and physiological characterization of AtGAAPs making use of the advanced knowledge of their human and viral counterparts. Structural modeling of AtGAAPs predicted the presence of a channel-like pore, and electrophysiological recordings from purified AtGAAP3 reconstituted into lipid bilayers confirmed that plant GAAPs can function as ion channels. AtGAAP1 and AtGAAP4 localized exclusively to the Golgi within the plant cell, while AtGAAP2, AtGAAP3 and AtGAAP5 also showed tonoplastic localization. Gene expression analysis revealed differential spatial expression and abundance of transcript forAtGAAPparalogues in Arabidopsis tissues. We demonstrate that AtGAAP1-5 inhibit Bax-induced cell death in yeast. However, overexpression of AtGAAP1 induces cell death inNicotiana benthamianaleaves and lesion mimic phenotype in Arabidopsis. We propose that AtGAAPs function as Golgi-localized ion channels that regulate cell death by affecting ionic homeostasis within the cell.HighlightArabidopsis Golgi anti-apoptotic proteins (GAAPs) share functional conservation with their human and viral counterparts in cell death regulation and ion channel activityAbbreviationsAtGAAP,Arabidopsis thalianaGAAP; BI-1, Bax inhibitor-1; CFP, cyan fluorescent protein; CMLV, camelpox virus; ER, Endoplasmic reticulum; GAAP, Golgi anti-apoptotic protein; GFP, green fluorescent protein; hGAAP, human GAAP; LFG, Lifeguard; LMM, lesion mimic mutant; PCD, programmed cell death; TMBIM, transmembrane Bax inhibitor-1 motif-containing; TMDs, transmembrane domains; vGAAP, viral GAAP; YFP, yellow fluorescent protein

Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis

2008 ◽  
Vol 32 (4) ◽  
pp. 599-609 ◽  
Author(s):  
Eva Ondroušková ◽  
Karel Souček ◽  
Viktor Horváth ◽  
Jan Šmarda
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Alternative Pathways ◽  
In Cells

scholarly journals Wild-Type Herpes Simplex Virus 1 Blocks Programmed Cell Death and Release of Cytochrome c but Not the Translocation of Mitochondrial Apoptosis-Inducing Factor to the Nuclei of Human Embryonic Lung Fibroblasts

2000 ◽  
Vol 74 (19) ◽  
pp. 9048-9053 ◽  
Author(s):  
Guoying Zhou ◽  
Bernard Roizman
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Infected Cell ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Human Embryonic Lung ◽  
Herpes Simplex Virus 1 ◽  
Infected Cells ◽  
In Cells

ABSTRACT Programmed cell death activated by herpes simplex virus 1 mutants can be caspase dependent or independent depending on the nature of the infected cell. The recently discovered mitochondrial apoptosis-inducing factor (AIF) on activation is translocated to the nucleus and induces programmed cell death that is caspase independent. To assess the role of AIF and also to assay apoptosis-related events in primary human embryonic lung (HEL) fibroblasts, cells were mock infected or infected with wild-type virus previously shown not to induce apoptosis in continuous lines of primate cells or with the d120 mutant lacking infected cell protein no. 4 (ICP4) and were shown to induce apoptosis in all cell lines tested. Cells exposed to dexamethasone or osmotic shock induced by sorbitol were the positive controls. The results were as follows: (i) AIF was translocated to the nucleus in all infected cell cultures and in cells treated with dexamethasone or sorbitol, but cells infected with the wild type-virus showed no evidence of undergoing programmed death. (ii) Cytochrome cwas released from mitochondria of cells infected with thed120 mutant or exposed to dexamethasone or sorbitol but not from mitochondria in cells treated with sorbitol and infected with the wild-type virus. (iii) Poly(ADP-ribose) polymerase was cleaved in mock-infected cells exposed to sorbitol or dexamethasone and in cells infected with the d120 mutant but not in either untreated cells infected with wild-type virus or cells exposed to sorbitol and then infected with wild-type virus. In contrast to HEp-2 cells, neitherd120 infection nor treatment with dexamethasone or sorbitol caused fragmentation of DNA in HEL fibroblasts. Electron microscopic examination showed chromatin condensation and vacuolization in a fraction of cells infected with d120 but not in wild-type virus-infected cells or cells treated with dexamethasone or sorbitol. We conclude that AIF is translocated to the nucleus in infected cells but apoptosis does not ensue in wild-type-infected cells. HEL fibroblasts infected with the d120 virus exhibit symptoms of classical apoptosis, such as cytochrome c release and cleavage of poly(ADP-ribose) polymerase observed also in cells undergoing caspase 3-dependent programmed cell death in which AIF is either not involved or not a contributory factor.

scholarly journals Ethylene Is One of the Key Elements for Cell Death and Defense Response Control in the Arabidopsis Lesion Mimic Mutant vad1

2007 ◽  
Vol 145 (2) ◽  
pp. 465-477 ◽  
Author(s):  
Olivier Bouchez ◽  
Carine Huard ◽  
Séverine Lorrain ◽  
Dominique Roby ◽  
Claudine Balagué
Keyword(s):  
Cell Death ◽  
Defense Response ◽  
Response Control ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant

Inhibition of Spleen Tyrosine Kinase with Fostamatinib Shows Pre-Clinical Activity Against Models of Waldenström Macroglobulinemia

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3723-3723
Author(s):  
Isere Kuiatse ◽  
Sheeba K. Thomas ◽  
Donna M. Weber ◽  
Adam M. Stein ◽  
Michael Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Tyrosine Kinase ◽  
Cell Line ◽  
Xenograft Model ◽  
Primary Cells ◽  
Spleen Tyrosine Kinase ◽  
Murine Xenograft Model ◽  
In Cells

Abstract Abstract 3723 Background: Waldenström macroglobulinemia (WM), a lymphoproliferative disorder with marrow infiltration by lymphoplasmacytic lymphoma cells and production of monoclonal IgM, is characterized clinically by good initial responses to standard therapeutic approaches. However, a minority of patients achieve a complete remission, and most inevitably relapse, indicating a need for validation of new, targeted therapies. Notably, B-cell receptor signaling has been linked to clonal evolution in WM, and Spleen tyrosine kinase (Syk) is over-expressed in primary patient cells. Also, a recent phase I/II study of the Syk inhibitor fostamatinib in patients with a variety of non-Hodgkin lymphomas showed evidence of activity in three patients with WM. These findings supported our central hypothesis, which proposed that Syk could be a rational new target for therapy of WM, which we pursued first with pre-clinical studies. Methods: Studies of fostamatinib were performed using the WM cell line MWCL-1, and the IgM-producing cell line BWCM.1, as well as in primary cells from patients with WM, and in a novel murine xenograft model utilizing MWCL-1 cells. Results: Fostamatinib induced a time- and dose-dependent reduction in viability of MWCL-1 and BWCM.1 cells, with median inhibitory concentrations (IC50) that were in the physiologically relevant range of approximately 0.25 and 1 μM, respectively, at 3 days. Cell cycle analysis showed a decrease in cells at S-phase and at G2/M, while an increase was seen in cells in G1, and in the sub-G1fraction, suggesting induction of apoptosis. Consistent with the possibility that there was activation of type I programmed cell death, increased staining was seen in fostamatinb-treated cells with an antibody to Annexin V. Interestingly, evidence was seen of the induction of type II programmed cell death, or autophagy, as measured by an increase in cells staining with the lysotropic dye acridine orange. At the molecular level, fostamatinib blocked signaling through p44/42 mitogen-activated protein kinase (MAPK), MAPK kinase (MEK), protein kinase B/Akt, and Zeta-chain-associated protein kinase (ZAP)-70/Syk, as judged by a reduction in the phosphorylated forms of these intermediates by Western blotting. Notably, the viability of primary cells isolated from patients with WM was also reduced in association with blockade of p44/42 MAPK. Finally, a novel murine xenograft model was generated by injection of MWCL-1 cells into immunodeficient mice, which developed measurable tumors. When these were treated with fostamatinib, a delay in tumor growth was demonstrable. Conclusions: Targeting Syk with fostamatinib is an attractive strategy against pre-clinical models of WM both in vitro and in vivo. These findings lend further support for translation of fostamatinib to the clinic for patients with relapsed, and possibly even newly diagnosed WM. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Proteome Analysis of Programmed Cell Death and Defense Signaling Using the Rice Lesion Mimic Mutant cdr2

2005 ◽  
Vol 18 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Hajime Tsunezuka ◽  
Masayuki Fujiwara ◽  
Tsutomu Kawasaki ◽  
Ko Shimamoto
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteome Analysis ◽  
Defense Responses ◽  
Spectrometric Analysis ◽  
Wild Type ◽  
High Accumulation ◽  
Defense Signaling ◽  
Lesion Mimic ◽  
Related Proteins

We have previously identified three lesion-mimic mutants, cell death and resistance (cdr), in rice. These mutants induce a series of defense responses, including expression of defense-related genes and high accumulation of phytoalexins, indicating that the cdr mutants are useful materials to study programmed cell death and defense signaling in rice. Here, we carried out a proteome analysis of the cdr2 mutant. Total proteins prepared from the wild type and the cdr2 mutant at three different stages of lesion formation were compared using two-dimensional electrophoresis. We found a total of 37 proteins that were differentially expressed between cdr2 and wild type. Among them, 28 spots were up-regulated and nine were down-regulated in the cdr2 mutant. All the protein spots were identified by mass spectrometric analysis. These differentially regulated proteins included defense-related proteins. In addition, 27 proteins were classified as metabolic enzymes, suggesting that the programmed cell death that occurs in the cdr2 mutant is associated with active metabolic changes. Our study shows that proteome analysis is a useful approach to study programmed cell death and defense signaling in plants.

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