scholarly journals Gene Mapping, Genome-Wide Transcriptome Analysis, and WGCNA Reveals the Molecular Mechanism for Triggering Programmed Cell Death in Rice Mutant pir1

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1607
Author(s):  
Xinyu Chen ◽  
Qiong Mei ◽  
Weifang Liang ◽  
Jia Sun ◽  
Xuming Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Biosynthesis Pathway ◽  
Wild Type ◽  
Biotic And Abiotic Stress ◽  
Alpha Linolenic Acid ◽  
Rice Mutant ◽  
Phenylpropanoid Biosynthesis ◽  
Physiological Analysis

Programmed cell death (PCD) is involved in plant growth and development and in resistance to biotic and abiotic stress. To understand the molecular mechanism that triggers PCD, phenotypic and physiological analysis was conducted using the first three leaves of mutant rice PCD-induced-resistance 1(pir1) and its wild-type ZJ22. The 2nd and 3rd leaves of pir1 had a lesion mimic phenotype, which was shown to be an expression of PCD induced by H2O2-accumulation. The PIR1 gene was mapped in a 498 kb-interval between the molecular markers RM3321 and RM3616 on chromosome 5, and further analysis suggested that the PCD phenotype of pir1 is controlled by a novel gene for rice PCD. By comparing the mutant with wild type rice, 1679, 6019, and 4500 differentially expressed genes (DEGs) were identified in the three leaf positions, respectively. KEGG analysis revealed that DEGs were most highly enriched in phenylpropanoid biosynthesis, alpha-linolenic acid metabolism, and brassinosteroid biosynthesis. In addition, conjoint analysis of transcriptome data by weighted gene co-expression network analysis (WGCNA) showed that the turquoise module of the 18 identified modules may be related to PCD. There are close interactions or indirect cross-regulations between the differential genes that are significantly enriched in the phenylpropanoid biosynthesis pathway and the hormone biosynthesis pathway in this module, which indicates that these genes may respond to and trigger PCD.

Proteome and metabolome profiling of wild-type and YCA1 -knock-out yeast cells during acetic acid-induced programmed cell death

2015 ◽  
Vol 128 ◽  
pp. 173-188 ◽  
Author(s):  
Valentina Longo ◽  
Maša Ždralević ◽  
Nicoletta Guaragnella ◽  
Sergio Giannattasio ◽  
Lello Zolla ◽  
...  
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Yeast Cells ◽  
Wild Type ◽  
Knock Out ◽  
Metabolome Profiling

scholarly journals Flight muscles degenerate by programmed cell death after migration in the wheat aphid, Sitobion avenae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Honglin Feng ◽  
Xiao Guo ◽  
Hongyan Sun ◽  
Shuai Zhang ◽  
Jinghui Xi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Differentially Expressed Genes ◽  
Flight Muscle ◽  
Sitobion Avenae ◽  
Differentially Expressed ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Muscle Degeneration ◽  
Flight Muscles

Abstract Objective Previous studies showed that flight muscles degenerate after migration in some aphid species; however, the underlying molecular mechanism remains virtually unknown. In this study, using the wheat aphid, Sitobion avenae, we aim to investigate aphid flight muscle degeneration and the underlying molecular mechanism. Results Sitobion avenae started to differentiate winged or wingless morphs at the second instar, the winged aphids were fully determined at the third instar, and their wings were fully developed at the fourth instar. After migration, the aphid flight muscles degenerated via programmed cell death, which is evidenced by a Terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling assay. Then, we identified a list of differentially expressed genes before and after tethered flights using differential-display reverse transcription-PCR. One of the differentially expressed genes, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following the aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration. During flight muscle degeneration, endogenous proteins may be degraded to reallocate energy for reproduction.

scholarly journals Transcriptome analysis of xa5-mediated resistance to bacterial leaf streak in rice (Oryza sativa L.)

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiaofang Xie ◽  
Zhiwei Chen ◽  
Binghui Zhang ◽  
Huazhong Guan ◽  
Yan Zheng ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanism ◽  
Oryza Sativa L ◽  
Blast Resistance ◽  
Rna Seq ◽  
Bacterial Leaf Streak ◽  
Wild Type ◽  
Cell Death Pathways ◽  
Rnai Line ◽  
Transgenic Lines

Abstract Bacterial leaf steak (BLS) caused by Xanthomonas oryzae pv. oryzicola (Xoc) is a devastating disease in rice production. The resistance to BLS in rice is a quantitatively inherited trait, of which the molecular mechanism is still unclear. It has been proved that xa5, a recessive bacterial blast resistance gene, is the most possible candidate gene of the QTL qBlsr5a for BLS resistance. To study the molecular mechanism of xa5 function in BLS resistance, we created transgenic lines with RNAi of Xa5 (LOC_Os05g01710) and used RNA-seq to analyze the transcriptomes of a Xa5-RNAi line and the wild-type line at 9 h after inoculation with Xoc, with the mock inoculation as control. We found that Xa5-RNAi could (1) increase the resistance to BLS as expected from xa5; (2) alter (mainly up-regulate) the expression of hundreds of genes, most of which were related to disease resistance; and (3) greatly enhance the response of thousands of genes to Xoc infection, especially of the genes involved in cell death pathways. The results suggest that xa5 is the cause of BLS-resistance of QTL qBlsr5a and it displays BLS resistance effect probably mainly because of the enhanced response of the cell death-related genes to Xoc infection.

Molecular mechanism of programmed cell death in the developing nervous system

1993 ◽  
pp. 23-31
Author(s):  
Eugene M. Johnson ◽  
Ellen B. Cornbrooks ◽  
Thomas L. Deckwerth ◽  
Steven Estus ◽  
James L. Franklin ◽  
...  
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Developing Nervous System

scholarly journals Lack ofHXK2Induces Localization of Active Ras in Mitochondria and Triggers Apoptosis in the YeastSaccharomyces cerevisiae

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Loredana Amigoni ◽  
Enzo Martegani ◽  
Sonia Colombo
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
Mitochondrial Dysfunction ◽  
Type Strain ◽  
Wild Type Strain ◽  
Ros Production ◽  
Ras Proteins ◽  
Wild Type

We recently showed that activated Ras proteins are localized to the plasma membrane and in the nucleus in wild-type cells growing exponentially on glucose, while in thehxk2Δ strain they accumulated mainly in mitochondria. An aberrant accumulation of activated Ras in these organelles was previously reported and correlated to mitochondrial dysfunction, accumulation of ROS, and cell death. Here we show that addition of acetic acid to wild-type cells results in a rapid recruitment of Ras-GTP from the nucleus and the plasma membrane to the mitochondria, providing a further proof that Ras proteins might be involved in programmed cell death. Moreover, we show that Hxk2 protects against apoptosis inS. cerevisiae. In particular, cells lackingHXK2and showing a constitutive accumulation of activated Ras at the mitochondria are more sensitive to acetic-acid-induced programmed cell death compared to the wild type strain. Indeed, deletion ofHXK2causes an increase of apoptotic cells with several morphological and biochemical changes that are typical of apoptosis, including DNA fragmentation, externalization of phosphatidylserine, and ROS production. Finally, our results suggest that apoptosis induced by lack of Hxk2 may not require the activation of Yca1, the metacaspase homologue identified in yeast.

scholarly journals Old Yellow Enzymes, Highly Homologous FMN Oxidoreductases with Modulating Roles in Oxidative Stress and Programmed Cell Death in Yeast

2007 ◽  
Vol 282 (49) ◽  
pp. 36010-36023 ◽  
Author(s):  
Osama Odat ◽  
Samer Matta ◽  
Hadi Khalil ◽  
Sotirios C. Kampranis ◽  
Raymond Pfau ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Antioxidant Activities ◽  
Ros Generation ◽  
Oxidized Glutathione ◽  
Wild Type ◽  
Antioxidant Genes ◽  
Knock Out ◽  
Chronological Aging

In a genetic screen to identify modifiers of Bax-dependent lethality in yeast, the C terminus of OYE2 was isolated based on its capacity to restore sensitivity to a Bax-resistant yeast mutant strain. Overexpression of full-length OYE2 suppresses Bax lethality in yeast, lowers endogenous reactive oxygen species (ROS), increases resistance to H2O2-induced programmed cell death (PCD), and significantly lowers ROS levels generated by organic prooxidants. Reciprocally, Δoye2 yeast strains are sensitive to prooxidant-induced PCD. Overexpression and knock-out analysis indicate these OYE2 antioxidant activities are opposed by OYE3, a highly homologous heterodimerizing protein, which functions as a prooxidant promoting H2O2-induced PCD in wild type yeast. To exert its effect OYE3 requires the presence of OYE2. Deletion of the 12 C-terminal amino acids and catalytic inactivation of OYE2 by a Y197F mutation enhance significantly survival upon H2O2-induced PCD in wild type cells, but accelerate PCD in Δoye3 cells, implicating the oye2p-oye3p heterodimer for promoting cell death upon oxidative stress. Unexpectedly, a strain with a double knock-out of these genes (Δoye2 oye3) is highly resistant to H2O2-induced PCD, exhibits increased respiratory capacity, and undergoes less cell death during the adaptive response in chronological aging. Simultaneous deletion of OYE2 and other antioxidant genes hyperinduces endogenous levels of ROS, promoting H2O2-induced cell death: in Δoye2 glr1 yeast high levels of oxidized glutathione elicited gross morphological aberrations involving the actin cytoskeleton and defects in organelle partitioning. Altering the ratio of reduced to oxidized glutathione by exogenous addition of GSH fully reversed these alterations. Based on this work, OYE proteins are firmly placed in the signaling network connecting ROS generation, PCD modulation, and cytoskeletal dynamics in yeast.

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 Molecular Mechanism of Food-Derived Polyphenols on PD-L1 Dimerization: A Molecular Dynamics Simulation Study

2021 ◽  
Vol 22 (20) ◽  
pp. 10924
Author(s):  
Yan Guo ◽  
Jianhuai Liang ◽  
Boping Liu ◽  
Yulong Jin
Keyword(s):  
Molecular Dynamics ◽  
Cell Death ◽  
Free Energy ◽  
Programmed Cell Death ◽  
Cancer Immunotherapy ◽  
Molecular Mechanism ◽  
Small Molecule ◽  
Small Molecule Inhibitors ◽  
Binding Free Energy ◽  
Dynamics Simulation

In cancer immunotherapy, an emerging approach is to block the interactions of programmed cell death-1 (PD-1) and programmed cell death-ligand 1 (PD-L1) using small-molecule inhibitors. The food-derived polyphenols curcumin (CC), res (RSV) and epigallocatechin gallate (EGCG) have anticancer immunologic functions, which, recently, have been proposed to act via the downregulation of PD-L1 expression. However, it remains unclear whether they can directly target PD-L1 dimerization and, thus, interrupt the PD-1/PD-L1 pathway. To elucidate the molecular mechanism of such compounds on PD-L1 dimerization, molecular docking and nanosecond molecular dynamics simulations were performed. Binding free energy calculations show that the affinities of CC, RSV and EGCG to the PD-L1 dimer follow a trend of CC > RSV > EGCG. Hence, CC is the most effective inhibitor of the PD-1/PD-L1 pathway. Analysis on contact numbers, nonbonded interactions and residue energy decomposition indicate that such compounds mainly interact with the C-, F- and G-sheet fragments of the PD-L1 dimer, which are involved in interactions with PD-1. More importantly, nonpolar interactions between these compounds and the key residues Ile54, Tyr56, Met115, Ala121 and Tyr123 play a dominant role in binding. Free energy landscape and secondary structure analyses further demonstrate that such compounds can stably interact with the binding domain of the PD-L1 dimer. The results provide evidence that CC, RSV and EGCG can inhibit PD-1/PD-L1 interactions by directly targeting PD-L1 dimerization. This provides a novel approach to discovering food-derived small-molecule inhibitors of the PD-1/PD-L1 pathway with potential applications in cancer immunotherapy.

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