scholarly journals The SAL-PAP Chloroplast Retrograde Pathway Contributes to Plant Immunity by Regulating Glucosinolate Pathway and Phytohormone Signaling

2017 ◽  
Vol 30 (10) ◽  
pp. 829-841 ◽  
Author(s):  
Yasuhiro Ishiga ◽  
Mutsumi Watanabe ◽  
Takako Ishiga ◽  
Takayuki Tohge ◽  
Takakazu Matsuura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Pseudomonas Syringae ◽  
Expression Profiles ◽  
Plant Immunity ◽  
Gene Expression Profiles ◽  
Nuclear Gene ◽  
Retrograde Signaling ◽  
Necrotrophic Pathogen ◽  
Nuclear Gene Expression

Chloroplasts have a crucial role in plant immunity against pathogens. Increasing evidence suggests that phytopathogens target chloroplast homeostasis as a pathogenicity mechanism. In order to regulate the performance of chloroplasts under stress conditions, chloroplasts produce retrograde signals to alter nuclear gene expression. Many signals for the chloroplast retrograde pathway have been identified, including chlorophyll intermediates, reactive oxygen species, and metabolic retrograde signals. Although there is a reasonably good understanding of chloroplast retrograde signaling in plant immunity, some signals are not well-understood. In order to understand the role of chloroplast retrograde signaling in plant immunity, we investigated Arabidopsis chloroplast retrograde signaling mutants in response to pathogen inoculation. sal1 mutants (fry1-2 and alx8) responsible for the SAL1-PAP retrograde signaling pathway showed enhanced disease symptoms not only to the hemibiotrophic pathogen Pseudomonas syringae pv. tomato DC3000 but, also, to the necrotrophic pathogen Pectobacterium carotovorum subsp. carotovorum EC1. Glucosinolate profiles demonstrated the reduced accumulation of aliphatic glucosinolates in the fry1-2 and alx8 mutants compared with the wild-type Col-0 in response to DC3000 infection. In addition, quantification of multiple phytohormones and analyses of their gene expression profiles revealed that both the salicylic acid (SA)- and jasmonic acid (JA)-mediated signaling pathways were down-regulated in the fry1-2 and alx8 mutants. These results suggest that the SAL1-PAP chloroplast retrograde pathway is involved in plant immunity by regulating the SA- and JA-mediated signaling pathways.

scholarly journals Mitochondrial TSPO Deficiency Triggers Retrograde Signaling in MA-10 Mouse Tumor Leydig Cells

2020 ◽  
Vol 22 (1) ◽  
pp. 252
Author(s):  
Jinjiang Fan ◽  
Vassilios Papadopoulos
Keyword(s):  
Gene Expression ◽  
Membrane Potential ◽  
Intracellular Signaling ◽  
Leydig Cells ◽  
Expression Profiles ◽  
Nuclear Gene ◽  
Retrograde Signaling ◽  
Mouse Tumor ◽  
Nuclear Gene Expression ◽  
Indel Mutation

The mitochondrial translocator protein (TSPO) has been shown to bind cholesterol with high affinity and is involved in mediating its availability for steroidogenesis. We recently reported that targeted Tspo gene deletion in MA-10 mouse tumor Leydig cells resulted in reduced cAMP-stimulated steroid formation and significant reduction in the mitochondrial membrane potential (ΔΨm) compared to control cells. We hypothesized that ΔΨm reduction in the absence of TSPO probably reflects the dysregulation and/or maintenance failure of some basic mitochondrial function(s). To explore the consequences of TSPO depletion via CRISPR-Cas9-mediated deletion (indel) mutation in MA-10 cells, we assessed the transcriptome changes in TSPO-mutant versus wild-type (Wt) cells using RNA-seq. Gene expression profiles were validated using real-time PCR. We report herein that there are significant changes in nuclear gene expression in Tspo mutant versus Wt cells. The identified transcriptome changes were mapped to several signaling pathways including the regulation of membrane potential, calcium signaling, extracellular matrix, and phagocytosis. This is a retrograde signaling pathway from the mitochondria to the nucleus and is probably the result of changes in expression of several transcription factors, including key members of the NF-κB pathway. In conclusion, TSPO regulates nuclear gene expression through intracellular signaling. This is the first evidence of a compensatory response to the loss of TSPO with transcriptome changes at the cellular level.

Distinct nuclear gene expression profiles in cells with mtDNA depletion and homoplasmic A3243G mutation

2005 ◽  
Vol 578 (1-2) ◽  
pp. 43-52 ◽  
Author(s):  
Roshan S. Jahangir Tafrechi ◽  
Peter J. Svensson ◽  
George M.C. Janssen ◽  
Karoly Szuhai ◽  
J. Antonie Maassen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Nuclear Gene ◽  
Mtdna Depletion ◽  
Nuclear Gene Expression ◽  
A3243g Mutation ◽  
In Cells

Gene expression profiles predict the possible regulatory role of OPN-mediated signaling pathways in rat liver regeneration

Gene ◽  
2016 ◽  
Vol 576 (2) ◽  
pp. 782-790 ◽  
Author(s):  
Gaiping Wang ◽  
Shasha Chen ◽  
Congcong Zhao ◽  
Xiaofang Li ◽  
Ling Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Regeneration ◽  
Signaling Pathways ◽  
Rat Liver ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Regulatory Role ◽  
Rat Liver Regeneration

scholarly journals Pectobacterium carotovorum Elicits Plant Cell Death with DspE/F but the P. carotovorum DspE Does Not Suppress Callose or Induce Expression of Plant Genes Early in Plant–Microbe Interactions

2011 ◽  
Vol 24 (7) ◽  
pp. 773-786 ◽  
Author(s):  
Hye-Sook Kim ◽  
Phanit Thammarat ◽  
Steven A. Lommel ◽  
Clifford S. Hogan ◽  
Amy O. Charkowski
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Secretion System ◽  
Broad Host Range ◽  
Pectobacterium Carotovorum ◽  
Callose Deposition

The broad-host-range bacterial soft rot pathogen Pectobacterium carotovorum causes a DspE/F-dependent plant cell death on Nicotiana benthamiana within 24 h postinoculation (hpi) followed by leaf maceration within 48 hpi. P. carotovorum strains with mutations in type III secretion system (T3SS) regulatory and structural genes, including the dspE/F operon, did not cause hypersensitive response (HR)-like cell death and or leaf maceration. A strain with a mutation in the type II secretion system caused HR-like plant cell death but no maceration. P. carotovorum was unable to impede callose deposition in N. benthamiana leaves, suggesting that P. carotovorum does not suppress this basal immunity function. Within 24 hpi, there was callose deposition along leaf veins and examination showed that the pathogen cells were localized along the veins. To further examine HR-like plant cell death induced by P. carotovorum, gene expression profiles in N. benthamiana leaves inoculated with wild-type and mutant P. carotovorum and Pseudomonas syringae strains were compared. The N. benthamiana gene expression profile of leaves infiltrated with Pectobacterium carotovorum was similar to leaves infiltrated with a Pseudomonas syringae T3SS mutant. These data support a model where Pectobacterium carotovorum uses the T3SS to induce plant cell death in order to promote leaf maceration rather than to suppress plant immunity.

scholarly journals Dact gene expression profiles suggest a role for this gene family in integrating Wnt and TGF-β signaling pathways during chicken limb development

2013 ◽  
Vol 243 (3) ◽  
pp. 428-439 ◽  
Author(s):  
Lucimara Aparecida Sensiate ◽  
Débora R. Sobreira ◽  
Fernanda Cristina Da Veiga ◽  
Denner Jefferson Peterlini ◽  
Angelica Vasconcelos Pedrosa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Family ◽  
Signaling Pathways ◽  
Limb Development ◽  
Expression Profiles ◽  
Gene Expression Profiles

scholarly journals Logic-based Analysis of Gene Expression Data Predicts Pathway Crosstalk between TNF, TGFB1 and EGF in Basal-like Breast Cancer

2019 ◽  
Author(s):  
Kyuri Jo ◽  
Beatriz Santos Buitrago ◽  
Minsu Kim ◽  
Sungmin Rhee ◽  
Carolyn Talcott ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Signaling Pathways ◽  
Expression Profiles ◽  
Formal System ◽  
Gene Expression Profiles ◽  
Breast Cancer Subtypes ◽  
Post Translational Modifications ◽  
Cancer Subtypes ◽  
Pathway Crosstalk

AbstractFor breast cancer, clinically important subtypes are well characterised at the molecular level in terms of gene expression profiles. In addition, signaling pathways in breast cancer have been extensively studied as therapeutic targets due to their roles in tumor growth and metastasis. However, it is challenging to put signaling pathways and gene expression profiles together to characterise biological mechanisms of breast cancer subtypes since many signaling events result from post-translational modifications, rather than gene expression differences.We present a logic-based approach to explain the differences in gene expression profiles among breast cancer subtypes using Pathway Logic and transcriptional network information. Pathway Logic is a rewriting-logic-based formal system for modeling biological pathways including post-translational modifications. Proposed method demonstrated its utility by constructing subtype-specific path from key receptors (TNFR, TGFBR1 and EGFR) to key transcription factor (TF) regulators (RELA, ATF2, SMAD3 and ELK1) and identifying potential pathway crosstalk via TFs in basal-specific paths, which could provide a novel insight on aggressive breast cancer subtypes.AvailabilityAnalysis result is available at http://epigenomics.snu.ac.kr/PL/

Identification of distinctive patterns in cell signaling pathways in glioblastoma multiforme subtypes using gene expression TCGA data sets.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23162-e23162
Author(s):  
Konstantin Volyanskyy ◽  
Minghao Zhong ◽  
Payal Keswarpu ◽  
John T Fallon ◽  
Michael Paul Fanucchi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Normal Tissue ◽  
Gene Selection ◽  
Molecular Subtype ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
The Cancer Genome Atlas ◽  
Cell Signaling Pathways

e23162 Background: Cancer is characterized by a variety of heterogeneous genomic and transcriptomic patterns involving highly complex signaling biological pathways. The problem of identification of the factors driving tumor progression becomes even more challenging due to intricate interaction mechanisms between these pathways. Using novel approaches in machine learning, we demonstrate the ability to quantitatively describe characteristic signaling patterns in cancer based on transcriptomic data Methods: We used RNASeq data from 20531 genes in 174 samples of GBM from The Cancer Genome Atlas including 5 major histological subtypes – Classical, G-CIMP, Mesenchymal, Neural, and Proneural, anddeveloped predictive computational framework for molecular subtype differentiation from normal tissue relying on variance based gene selection and random forest algorithm. Results: We obtained a few key findings – (1) genes from cell signaling pathways alone differentiate each subtype from normal tissue with 100% accuracy; (2) predictive genes are specific to each subtype; (3) inferred pathway interactions are also specific to each subtype; (4) typically most of the predictive genes involved in signaling are down-regulated in tumor compared to normal tissue (MAPT, PRKCG, PDE2A, RYR2, ATP1B1, GRN1, GNAO1), however, in each subtype we observed a smaller subset of predictive genes which are highly up-regulated in tumor (ID3, FN1, JAG1, F2R, COL4A1, EDAR, CDK2, CDK4, MFNG, BIRC5, CCNB2). We detected and quantitatively evaluated characteristic signaling pathway involvement across the GBM subtypes for MAPK, RAP1, RAS, Notch, PI3K-Akt, mTOR, FoxO, Jak-STAT, Wnt, cAMP, and Calcium Signaling, providing a unique approximation for each subtype signaling profile. Conclusions: In this study, we identified gene expression profiles and associated signaling pathways for distinguishing GBM Multiforme subtypes from normal tissue. We observed and described a dense complex picture of interacting signaling pathways. The detected interactions may provide clinical insights and could be used to identify potential therapeutic targets, however, more research is needed to confirm this.

scholarly journals HnRNPA2 is a novel histone acetyltransferase that mediates mitochondrial stress-induced nuclear gene expression

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Manti Guha ◽  
Satish Srinivasan ◽  
Kip Guja ◽  
Edison Mejia ◽  
Miguel Garcia-Diaz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dna ◽  
Transcriptional Activation ◽  
Nuclear Gene ◽  
C2c12 Cells ◽  
Retrograde Signaling ◽  
Epigenetic Mechanism ◽  
Mitochondrial Stress ◽  
Nuclear Gene Expression ◽  
Mitochondrial Dna Copy Number

Abstract Reduced mitochondrial DNA copy number, mitochondrial DNA mutations or disruption of electron transfer chain complexes induce mitochondria-to-nucleus retrograde signaling, which induces global change in nuclear gene expression ultimately contributing to various human pathologies including cancer. Recent studies suggest that these mitochondrial changes cause transcriptional reprogramming of nuclear genes although the mechanism of this cross talk remains unclear. Here, we provide evidence that mitochondria-to-nucleus retrograde signaling regulates chromatin acetylation and alters nuclear gene expression through the heterogeneous ribonucleoprotein A2 (hnRNAP2). These processes are reversed when mitochondrial DNA content is restored to near normal cell levels. We show that the mitochondrial stress-induced transcription coactivator hnRNAP2 acetylates Lys 8 of H4 through an intrinsic histone lysine acetyltransferase (KAT) activity with Arg 48 and Arg 50 of hnRNAP2 being essential for acetyl-CoA binding and acetyltransferase activity. H4K8 acetylation at the mitochondrial stress-responsive promoters by hnRNAP2 is essential for transcriptional activation. We found that the previously described mitochondria-to-nucleus retrograde signaling-mediated transformation of C2C12 cells caused an increased expression of genes involved in various oncogenic processes, which is retarded in hnRNAP2 silenced or hnRNAP2 KAT mutant cells. Taken together, these data show that altered gene expression by mitochondria-to-nucleus retrograde signaling involves a novel hnRNAP2-dependent epigenetic mechanism that may have a role in cancer and other pathologies.

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