scholarly journals Multiple insertions of COIN , a novel maize Foldback transposable element, in the Conring gene cause a spontaneous progressive cell death phenotype

2020 ◽  
Vol 104 (3) ◽  
pp. 581-595
Author(s):  
Saet‐Byul Kim ◽  
Shailesh Karre ◽  
Qingyu Wu ◽  
Minkyu Park ◽  
Emily Meyers ◽  
...  
Keyword(s):  
Cell Death ◽  
Transposable Element ◽  
Cell Death Phenotype

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

scholarly journals Inhibition of RNA Interference and Modulation of Transposable Element Expression by Cell Death in Drosophila

Genetics ◽  
2011 ◽  
Vol 188 (4) ◽  
pp. 823-834 ◽  
Author(s):  
Weiwu Xie ◽  
Chengzhi Liang ◽  
James A. Birchler
Keyword(s):  
Cell Death ◽  
Rna Interference ◽  
Transposable Element

scholarly journals Arabidopsis ssi2-Conferred Susceptibility to Botrytis cinerea Is Dependent on EDS5 and PAD4

2005 ◽  
Vol 18 (4) ◽  
pp. 363-370 ◽  
Author(s):  
Ashis Nandi ◽  
Wolfgang Moeder ◽  
Pradeep Kachroo ◽  
Daniel F. Klessig ◽  
Jyoti Shah
Keyword(s):  
Cell Death ◽  
Botrytis Cinerea ◽  
Pseudomonas Syringae ◽  
Desaturase Activity ◽  
Peronospora Parasitica ◽  
Basal Resistance ◽  
Enhanced Resistance ◽  
Pathogenesis Related ◽  
Cell Death Phenotype ◽  
Dependent Mechanism

Loss of a stearoyl-ACP desaturase activity in the Arabidopsis thaliana ssi2 mutant confers susceptibility to the necrotroph, Botrytis cinerea. In contrast, the ssi2 mutant exhibits enhanced resistance to Pseudomonas syringae, Peronospora parasitica, and Cucumber mosaic virus. The altered basal resistance to these pathogens in the ssi2 mutant plant is accompanied by the constitutive accumulation of elevated salicylic acid (SA) level and expression of the pathogenesis-related 1 (PR1) gene, the inability of jasmonic acid (JA) to activate expression of the defensin gene, PDF1.2, and the spontaneous death of cells. Here, we show that presence of the eds5 and pad4 mutant alleles compromises the ssi2-conferred resistance to Pseudomonas syringae pv. maculicola. In contrast, resistance to B. cinerea was restored in the ssi2 eds5 and ssi2 pad4 double-mutant plants. However, resistance to B. cinerea was not accompanied by the restoration of JA responsiveness in the ssi2 eds5 and ssi2 pad4 plants. The ssi2 eds5 and ssi2 pad4 plants retain the ssi2-conferred spontaneous cell death phenotype, suggesting that cell death is not a major factor that predisposes the ssi2 mutant to infection by B. cinerea. Furthermore, the high SA content of the ssi2 pad4 plant, combined with our previous observation that the SA-deficient ssi2 nahG plant succumbs to infection by B. cinerea, suggests that elevated SA level does not have a causal role in the ssi2-conferred susceptibility to B. cinerea. Our results suggest that interaction between an SSI2-dependent factor or factors and an EDS5- and PAD4- dependent mechanism or mechanisms modulates defense to B. cinerea.

scholarly journals Suppressors of the Arabidopsis lsd5 Cell Death Mutation Identify Genes Involved in Regulating Disease Resistance Responses

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 305-319
Author(s):  
Jean-Benoit Morel ◽  
Jeffery L Dangl
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Plant Disease Resistance ◽  
Plant Disease ◽  
Disease Susceptibility ◽  
Bacterial Pathogen ◽  
Hypersensitive Reaction ◽  
Cell Death Phenotype ◽  
New Mutations

Abstract Cell death is associated with the development of the plant disease resistance hypersensitive reaction (HR). Arabidopsis lsd mutants that spontaneously exhibit cell death reminiscent of the HR were identified previously. To study further the regulatory context in which cell death acts during disease resistance, one of these mutants, lsd5, was used to isolate new mutations that suppress its cell death phenotype. Using a simple lethal screen, nine lsd5 cell death suppressors, designated phx (for the mythological bird Phoenix that rises from its ashes), were isolated. These mutants were characterized with respect to their response to a bacterial pathogen and oomycete parasite. The strongest suppressors—phx2, 3, 6, and 11-1—showed complex, differential patterns of disease resistance modifications. These suppressors attenuated disease resistance to avirulent isolates of the biotrophic Peronospora parasitica pathogen, but only phx2 and phx3 altered disease resistance to avirulent strains of Pseudomonas syringae pv tomato. Therefore, some of these phx mutants define common regulators of cell death and disease resistance. In addition, phx2 and phx3 exhibited enhanced disease susceptibility to different virulent pathogens, confirming probable links between the disease resistance and susceptibility pathways.

scholarly journals Cell death phenotype of vacuole Ca2+-ATPase11 (ACA11) transgenic plant in Arabidopsis

2009 ◽  
Vol 36 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Sang-Min Lee ◽  
My-HanhThi Hoang ◽  
Kyung-Eun Kim ◽  
Woo-Sik Chung
Keyword(s):  
Cell Death ◽  
Transgenic Plant ◽  
Cell Death Phenotype

scholarly journals N-Methyl-D-Aspartate Receptor Hypofunction in Meg-01 Cells Reveals a Role for Intracellular Calcium Homeostasis in Balancing Megakaryocytic-Erythroid Differentiation

2020 ◽  
Vol 120 (04) ◽  
pp. 671-686 ◽  
Author(s):  
James I. Hearn ◽  
Taryn N. Green ◽  
Martin Chopra ◽  
Yohanes N. S. Nursalim ◽  
Leandro Ladvanszky ◽  
...  
Keyword(s):  
Cell Death ◽  
Er Stress ◽  
Erythroid Differentiation ◽  
Alternative Source ◽  
Cytotoxic Effects ◽  
Dense Granules ◽  
Aspartate Receptor ◽  
Store Operated Calcium Entry ◽  
Lysosome Related Organelles ◽  
Cell Death Phenotype

AbstractThe release of calcium ions (Ca2+) from the endoplasmic reticulum (ER) and related store-operated calcium entry (SOCE) regulate maturation of normal megakaryocytes. The N-methyl-D-aspartate (NMDA) receptor (NMDAR) provides an additional mechanism for Ca2+ influx in megakaryocytic cells, but its role remains unclear. We created a model of NMDAR hypofunction in Meg-01 cells using CRISPR-Cas9 mediated knockout of the GRIN1 gene, which encodes an obligate, GluN1 subunit of the NMDAR. We found that compared with unmodified Meg-01 cells, Meg-01-GRIN1 −/− cells underwent atypical differentiation biased toward erythropoiesis, associated with increased basal ER stress and cell death. Resting cytoplasmic Ca2+ levels were higher in Meg-01-GRIN1 −/− cells, but ER Ca2+ release and SOCE were lower after activation. Lysosome-related organelles accumulated including immature dense granules that may have contributed an alternative source of intracellular Ca2+. Microarray analysis revealed that Meg-01-GRIN1 −/− cells had deregulated expression of transcripts involved in Ca2+ metabolism, together with a shift in the pattern of hematopoietic transcription factors toward erythropoiesis. In keeping with the observed pro-cell death phenotype induced by GRIN1 deletion, memantine (NMDAR inhibitor) increased cytotoxic effects of cytarabine in unmodified Meg-01 cells. In conclusion, NMDARs comprise an integral component of the Ca2+ regulatory network in Meg-01 cells that help balance ER stress and megakaryocytic-erythroid differentiation. We also provide the first evidence that megakaryocytic NMDARs regulate biogenesis of lysosome-related organelles, including dense granules. Our results argue that intracellular Ca2+ homeostasis may be more important for normal megakaryocytic and erythroid differentiation than currently recognized; thus, modulation may offer therapeutic opportunities.

scholarly journals Sphingolipid-Induced Programmed Cell Death Is a Salicylic Acid and EDS1-Dependent Phenotype in Arabidopsis

2021 ◽  
Author(s):  
Stefanie Koenig ◽  
Jasmin Goemann ◽  
Agnieszka Zienkiewicz ◽  
Krzysztof Zienkiewicz ◽  
Dorothea Meldau ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Programmed Cell Death ◽  
Sphingolipid Metabolism ◽  
Ceramide Synthase ◽  
Triple Mutant ◽  
A Cell ◽  
P Fraction ◽  
Chain Lengths ◽  
Cell Death Phenotype

Ceramides and long chain bases (LCBs) are plant sphingolipids involved in the induction of plant programmed cell death (PCD). The fatty acid hydroxylase mutant fah1 fah2 exhibits high ceramide levels and moderately elevated LCB levels. Salicylic acid (SA) is strongly induced in these mutants, but no cell death is visible. To determine the effect of ceramides with different chain lengths, fah1 fah2 was crossed with ceramide synthase mutants longevity assurance gene one homologue1-3 (loh1, loh2 and loh3). Surprisingly, only triple mutants with loh2 show a cell death phenotype under the selected conditions. Sphingolipid profiling revealed that the greatest differences between the triple mutant plants are in the LCB and LCB-phosphate (LCB-P) fraction. fah1 fah2 loh2 plants accumulate LCB d18:0 and LCB-P d18:0. Crossing fah1 fah2 loh2 with the SA synthesis mutant sid2-2, and with the SA signaling mutants enhanced disease susceptibility 1-2 (eds1-2) and phytoalexin deficient 4-1 (pad4-1), revealed that lesions are SA- and EDS1-dependent. These quadruple mutants also suggest that there may be a feedback loop between SA and sphingolipid metabolism as they accumulated less ceramides and LCBs. In conclusion, PCD in fah1 fah2 loh2 is a SA and EDS1-dependent phenotype, which is likely due to accumulation of LCB d18:0.

scholarly journals Loss of the common immune coreceptor BAK1 leads to NLR-dependent cell death

2020 ◽  
Vol 117 (43) ◽  
pp. 27044-27053 ◽  
Author(s):  
Yujun Wu ◽  
Yang Gao ◽  
Yanyan Zhan ◽  
Hong Kui ◽  
Hongyan Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Receptor Protein ◽  
Dependent Manner ◽  
Effector Triggered Immunity ◽  
Dependent Cell ◽  
A Cell ◽  
Cell Death Phenotype ◽  
Recognition Receptor

Plants utilize a two-tiered immune system consisting of pattern recognition receptor (PRR)-triggered immunity (PTI) and effector-triggered immunity (ETI) to defend themselves against pathogenic microbes. The receptor protein kinase BAK1 plays a central role in multiple PTI signaling pathways in Arabidopsis. However, double mutants made by BAK1 and its closest paralog BKK1 exhibit autoimmune phenotypes, including cell death resembling a typical nucleotide-binding leucine-rich repeat protein (NLR)-mediated ETI response. The molecular mechanisms of the cell death caused by the depletion of BAK1 and BKK1 are poorly understood. Here, we show that the cell-death phenotype of bak1 bkk1 is suppressed when a group of NLRs, ADR1s, are mutated, indicating the cell-death of bak1 bkk1 is the consequence of NLR activation. Furthermore, introduction of a Pseudomonas syringae effector HopB1, which proteolytically cleaves activated BAK1 and its paralogs via either gene transformation or bacterium-delivery, results in a cell-death phenotype in an ADR1s-dependent manner. Our study thus pinpoints that BAK1 and its paralogs are likely guarded by NLRs.

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