scholarly journals A Transcriptomic Approach Provides Insights on the Mycorrhizal Symbiosis of the Mediterranean Orchid Limodorum abortivum in Nature

Plants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 251
Author(s):  
Rafael B. S. Valadares ◽  
Fabio Marroni ◽  
Fabiano Sillo ◽  
Renato R. M. Oliveira ◽  
Raffaella Balestrini ◽  
...  
Keyword(s):  
Gene Expression ◽  
Common Core ◽  
Mycorrhizal Symbiosis ◽  
Marker Genes ◽  
Plant Responses ◽  
Orchid Mycorrhiza ◽  
Orchid Species ◽  
Plant Genes ◽  
Mycorrhizal Roots ◽  
Mycorrhizal Interactions

The study of orchid mycorrhizal interactions is particularly complex because of the peculiar life cycle of these plants and their diverse trophic strategies. Here, transcriptomics has been applied to investigate gene expression in the mycorrhizal roots of Limodorum abortivum, a terrestrial mixotrophic orchid that associates with ectomycorrhizal fungi in the genus Russula. Our results provide new insights into the mechanisms underlying plant–fungus interactions in adult orchids in nature and in particular into the plant responses to the mycorrhizal symbiont(s) in the roots of mixotrophic orchids. Our results indicate that amino acids may represent the main nitrogen source in mycorrhizal roots of L. abortivum, as already suggested for orchid protocorms and other orchid species. The upregulation, in mycorrhizal L. abortivum roots, of some symbiotic molecular marker genes identified in mycorrhizal roots from other orchids as well as in arbuscular mycorrhiza, may mirror a common core of plant genes involved in endomycorrhizal symbioses. Further efforts will be required to understand whether the specificities of orchid mycorrhiza depend on fine-tuned regulation of these common components, or whether specific additional genes are involved.

scholarly journals Multi-view feature selection for identifying gene markers: a diversified biological data driven approach

2020 ◽  
Vol 21 (S18) ◽  
Author(s):  
Sudipta Acharya ◽  
Laizhong Cui ◽  
Yi Pan
Keyword(s):  
Gene Expression ◽  
Feature Selection ◽  
Gene Selection ◽  
Marker Gene ◽  
Biological Data ◽  
Protein Interaction Data ◽  
Marker Genes ◽  
Data Sets ◽  
Gene Markers ◽  
Multi Objective

Abstract Background In recent years, to investigate challenging bioinformatics problems, the utilization of multiple genomic and proteomic sources has become immensely popular among researchers. One such issue is feature or gene selection and identifying relevant and non-redundant marker genes from high dimensional gene expression data sets. In that context, designing an efficient feature selection algorithm exploiting knowledge from multiple potential biological resources may be an effective way to understand the spectrum of cancer or other diseases with applications in specific epidemiology for a particular population. Results In the current article, we design the feature selection and marker gene detection as a multi-view multi-objective clustering problem. Regarding that, we propose an Unsupervised Multi-View Multi-Objective clustering-based gene selection approach called UMVMO-select. Three important resources of biological data (gene ontology, protein interaction data, protein sequence) along with gene expression values are collectively utilized to design two different views. UMVMO-select aims to reduce gene space without/minimally compromising the sample classification efficiency and determines relevant and non-redundant gene markers from three cancer gene expression benchmark data sets. Conclusion A thorough comparative analysis has been performed with five clustering and nine existing feature selection methods with respect to several internal and external validity metrics. Obtained results reveal the supremacy of the proposed method. Reported results are also validated through a proper biological significance test and heatmap plotting.

scholarly journals Metabolomics and transcriptomics to decipher molecular mechanisms underlying ectomycorrhizal root colonization of an oak tree

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
M. Sebastiana ◽  
A. Gargallo-Garriga ◽  
J. Sardans ◽  
M. Pérez-Trujillo ◽  
F. Monteiro ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Positive Impact ◽  
Ectomycorrhizal Fungus ◽  
Cork Oak ◽  
Mycorrhizal Symbiosis ◽  
Gamma Aminobutyric Acid ◽  
Ectomycorrhizal Symbiosis ◽  
Ectomycorrhizal Roots ◽  
Oak Tree ◽  
Mycorrhizal Roots

AbstractMycorrhizas are known to have a positive impact on plant growth and ability to resist major biotic and abiotic stresses. However, the metabolic alterations underlying mycorrhizal symbiosis are still understudied. By using metabolomics and transcriptomics approaches, cork oak roots colonized by the ectomycorrhizal fungus Pisolithus tinctorius were compared with non-colonized roots. Results show that compounds putatively corresponding to carbohydrates, organic acids, tannins, long-chain fatty acids and monoacylglycerols, were depleted in ectomycorrhizal cork oak colonized roots. Conversely, non-proteogenic amino acids, such as gamma-aminobutyric acid (GABA), and several putative defense-related compounds, including oxylipin-family compounds, terpenoids and B6 vitamers were induced in mycorrhizal roots. Transcriptomic analysis suggests the involvement of GABA in ectomycorrhizal symbiosis through increased synthesis and inhibition of degradation in mycorrhizal roots. Results from this global metabolomics analysis suggest decreases in root metabolites which are common components of exudates, and in compounds related to root external protective layers which could facilitate plant-fungal contact and enhance symbiosis. Root metabolic pathways involved in defense against stress were induced in ectomycorrhizal roots that could be involved in a plant mechanism to avoid uncontrolled growth of the fungal symbiont in the root apoplast. Several of the identified symbiosis-specific metabolites, such as GABA, may help to understand how ectomycorrhizal fungi such as P. tinctorius benefit their host plants.

scholarly journals Elevation of gene expression of Btg2, Gadd 153, and antioxidant markers in RONS-induced PC12 cells

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Aravind P ◽  
Sarojini R. Bulbule ◽  
Hemalatha N ◽  
Anushree G ◽  
Babu R.L ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Protein Expression ◽  
Pc12 Cells ◽  
Expression Pattern ◽  
High Glucose ◽  
Nitrosative Stress ◽  
Gene Expression Pattern ◽  
Marker Genes ◽  
Differential Stress

Abstract Background Free radicals generated in the biological system bring about modifications in biological molecules causing damage to their structure and function. Identifying the damage caused by ROS and RNS is important to predict the pathway of apoptosis due to stress in PC12 cells. The first defense mechanisms against them are antioxidants which act in various pathways through important cellular organelles like the mitochondria and endoplasmic reticulum. Specific biomarkers like Gadd153 which is a marker for endoplasmic reticulum stress, Nrf2 which responds to the redox changes and translocates the antioxidant response elements, and Btg2 which is an antioxidant regulator have not been addressed in different stress conditions previously in PC12 cells. Therefore, the study was conducted to analyze the gene expression pattern (SOD, Catalase, Btg2, Gadd153, and Nrf2) and the protein expression pattern (iNOS and MnSOD) of the antioxidant stress markers in differential stress-induced PC12 cells. Peroxynitrite (1 μM), rotenone (1 μM), H2O2(100 mM), and high glucose (33 mM) were used to induce oxidative and nitrosative stress in PC12 cells. Results The results obtained suggested that rotenone-induced PC12 cells showed a significant increase in the expression of catalase, Btg2, and Gadd153 compared to the control. Peroxynitrite-induced PC12 cells showed higher expression of Btg2 compared to the control. H2O2 and high glucose showed lesser expression compared to the control in all stress marker genes. In contrast, the Nrf2 gene expression is downregulated in all the stress-induced PC12 cells compared to the control. Further, MnSOD and iNOS protein expression studies suggest that PC12 cells exhibit a selective downregulation. Lower protein expression of MnSOD and iNOS may be resulted due to the mitochondrial dysfunction in peroxynitrite-, high glucose-, and H2O2-treated cells, whereas rotenone-induced cells showed lower expression, which could be the result of a dysfunction of the endoplasmic reticulum. Conclusion Different stress inducers like rotenone, peroxynitrite, H2O2, and high glucose increase the NO and ROS. Btg2 and Gadd153 genes were upregulated in the stress-induced cells, whereas the Nrf2 was significantly downregulated in differential stress-induced PC12 cells. Further, antioxidant marker genes were differentially expressed with different stress inducers.

scholarly journals Connectivity Map-based discovery of parbendazole reveals targetable human osteogenic pathway

2015 ◽  
Vol 112 (41) ◽  
pp. 12711-12716 ◽  
Author(s):  
Andrea M. Brum ◽  
Jeroen van de Peppel ◽  
Cindy S. van der Leije ◽  
Marijke Schreuders-Koedam ◽  
Marco Eijken ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Osteoblast Differentiation ◽  
Target Genes ◽  
Focal Adhesions ◽  
Bone Fragility ◽  
Bone Morphogenetic Protein 2 ◽  
Marker Genes ◽  
Connectivity Map ◽  
Morphogenetic Protein

Osteoporosis is a common skeletal disorder characterized by low bone mass leading to increased bone fragility and fracture susceptibility. In this study, we have identified pathways that stimulate differentiation of bone forming osteoblasts from human mesenchymal stromal cells (hMSCs). Gene expression profiling was performed in hMSCs differentiated toward osteoblasts (at 6 h). Significantly regulated genes were analyzed in silico, and the Connectivity Map (CMap) was used to identify candidate bone stimulatory compounds. The signature of parbendazole matches the expression changes observed for osteogenic hMSCs. Parbendazole stimulates osteoblast differentiation as indicated by increased alkaline phosphatase activity, mineralization, and up-regulation of bone marker genes (alkaline phosphatase/ALPL, osteopontin/SPP1, and bone sialoprotein II/IBSP) in a subset of the hMSC population resistant to the apoptotic effects of parbendazole. These osteogenic effects are independent of glucocorticoids because parbendazole does not up-regulate glucocorticoid receptor (GR) target genes and is not inhibited by the GR antagonist mifepristone. Parbendazole causes profound cytoskeletal changes including degradation of microtubules and increased focal adhesions. Stabilization of microtubules by pretreatment with Taxol inhibits osteoblast differentiation. Parbendazole up-regulates bone morphogenetic protein 2 (BMP-2) gene expression and activity. Cotreatment with the BMP-2 antagonist DMH1 limits, but does not block, parbendazole-induced mineralization. Using the CMap we have identified a previously unidentified lineage-specific, bone anabolic compound, parbendazole, which induces osteogenic differentiation through a combination of cytoskeletal changes and increased BMP-2 activity.

The influence of apple- and red-wine pomace rich diet on mRNA expression of inflammatory and apoptotic markers in different piglet organs

2006 ◽  
Vol 82 (6) ◽  
pp. 877-887 ◽  
Author(s):  
J. Sehm ◽  
H. Lindermayer ◽  
H. H. D. Meyer ◽  
M. W. Pfaffl
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Caspase 3 ◽  
Red Wine ◽  
Marker Genes ◽  
Apoptotic Marker ◽  
Mrna Gene ◽  
Turn Over ◽  
Mrna Gene Expression

Flavan-3-ols are a class of flavonoids that are widely distributed in fruits and beverages including red wine and apples. Consumption of flavanoid-rich food has been shown to exhibit anti-microbial, anti-oxidative, anti-inflammatory, and immune-modulating effects. To test the nutritional effects of flavanols on mRNA gene-expression of inflammatory and apoptotic marker genes, piglets were given two flavanoids-rich feeding regimens: a low flavanoid standard diet (SD) was compared with diets enriched with 3·5% apple pomace (APD) or 3·5% red-wine pomace (RWPD). The influence on mRNA expression levels was investigated in different immunological active tissues and in the gastro-intestinal tract (GIT). The investigation took place from 1 week prior weaning to 19 days post weaning in 78 piglets. The expression of expressed marker genes was determinate by one-step quantitative real-time (qRT-PCR): TNFα, NFκB as pro-inflammatory; IL10, as anti-inflammatory; caspase 3 as apoptosis; cyclin D1 as cell cycle marker; and nucleosome component histon H3 as reference gene.The feeding regimens result in tissue individual regulation of mRNA gene expression in all investigated organs. It was discovered that there were significant differences between the applied diets and significant changes during feeding time curse. Both pomace treatments caused a significant up-regulation of all investigated genes in liver. The effect on mesenterial lymph nodes and spleen was not prominent. In the GIT, the treatment groups showed a inhibitory effects on gene expression mainly in stomach and jejunum (NFκB, cyclin D1 and caspase 3). In colon the trend of caspase 3 was positive with the greatest change in the RWPD group.In jejunum and stomach the cell cycle turn over was reduced, whereas in liver the cell turn over was highly accelerate. The influence on inflammatory marker gene expression is mainly relevant in stomach. It is presume that both flavanoid rich feeding regimens have the potential to modulate the mRNA expressions of inflammatory, proliferation and apoptotic marker genes in the GIT and piglet organs.

Protein phosphatase 2A potentiates activity of promoters containing AP-1-binding elements

1993 ◽  
Vol 13 (4) ◽  
pp. 2104-2112
Author(s):  
A S Alberts ◽  
T Deng ◽  
A Lin ◽  
J L Meinkoth ◽  
A Schönthal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reporter Gene ◽  
Protein Phosphatase ◽  
Signal Transduction Pathways ◽  
Marker Genes ◽  
Direct Mechanism ◽  
Phosphatase 2A ◽  
Beta Galactosidase ◽  
Regulatory Sites

The involvement of serine/threonine protein phosphatases in signaling pathways which modulate the activity of the transcription factor AP-1 was examined. Purified protein phosphatase types 1 (PP1) and 2A (PP2A) were microinjected into cell lines containing stably transfected lacZ marker genes under the control of an enhancer recognized by AP-1. Microinjection of PP2A potentiated serum-stimulated beta-galactosidase expression from the AP-1-regulated promoter. Similarly, transient expression of the PP2A catalytic subunit with c-Jun resulted in a synergistic transactivation of an AP-1-regulated reporter gene. PP2A, but not PP1, potentiated serum-induced c-Jun expression, which has been previously shown to be autoregulated by AP-1 itself. Consistent with these results, PP2A dephosphorylated c-Jun on negative regulatory sites in vitro, suggesting one possible direct mechanism for the effects of PP2A on AP-1 activity. Microinjection of PP2A had no effect on cyclic AMP (cAMP)-induced expression of a reporter gene containing a cAMP-regulated promoter, while PP1 injection abolished cAMP-induced gene expression. Taken together, these results suggest a specific role for PP2A in signal transduction pathways that regulate AP-1 activity and c-Jun expression.

scholarly journals Gastric Cancer Cell Lines Have DifferentMYC-Regulated Expression Patterns but Share a Common Core of Altered Genes

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Jersey Heitor da S. Maués ◽  
Helem Ferreira Ribeiro ◽  
Giovanny R. Pinto ◽  
Luana de Oliveira Lopes ◽  
Letícia M. Lamarão ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Common Core ◽  
Gastric Cancer Cell ◽  
Histological Subtypes ◽  
Gene Sets ◽  
Regulated Expression ◽  
Gastric Cancer Cell Lines

MYCis an oncogene responsible for excessive cell growth in cancer, enabling transcriptional activation of genes involved in cell cycle regulation, metabolism, and apoptosis, and is usually overexpressed in gastric cancer (GC). By using siRNA and Next-Generation Sequencing (NGS), we identifiedMYC-regulated differentially expressed Genes (DEGs) in three Brazilian gastric cancer cell lines representing the histological subtypes of GC (diffuse, intestinal, and metastasis). The DEGs were picked usingSailfishsoftware, followed by Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis using KEGG. We found 11 significantly enriched gene sets by using enrichment score (ES), False Discovery Rate (FDR), and nominal P-values. We identified a total of 5.471 DEGs with correlation over (80%). In diffuse-type and in metastatic GC cell lines,MYC-silencing caused DEGs downregulation, while the intestinal-type GC cells presented overall DEGs upregulation afterMYCsiRNA depletion. We were able to detect 11 significant gene sets when comparing our samples to the hallmark collection of gene expression, enriched mostly for the following hallmarks: proliferation, pathway, signaling, metabolic, and DNA damage response. When we analyzed our DEGs considering KEGG metabolic pathways, we found 12 common branches covering a wide range of biological functions, and three of them were common to all three cell lines: ubiquitin-mediated proteolysis, ribosomes, and system and epithelial cell signaling inHelicobacter pyloriinfection. The GC cell lines used in this study share 14MYC-regulated genes, but their gene expression profile is different for each histological subtype of GC. Our results present a computational analysis ofMYC-related signatures in GC, and we present evidence that GC cell lines representing distinct histological subtypes of this disease have differentMYC-regulated expression profiles but share a common core of altered genes. This is an important step towards the understanding ofMYC’s role in gastric carcinogenesis and an indication of probable new drug targets in stomach cancer.

scholarly journals Analysis of brain atrophy and local gene expression in genetic frontotemporal dementia

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Andre Altmann ◽  
David M Cash ◽  
Martina Bocchetta ◽  
Carolin Heller ◽  
Regina Reynolds ◽  
...  
Keyword(s):  
Gene Expression ◽  
Frontotemporal Dementia ◽  
Cell Function ◽  
Neurodegenerative Disorder ◽  
Positive Association ◽  
Negative Association ◽  
Marker Genes ◽  
Gene Set ◽  
Genetic Groups ◽  
Cortical Regions

Abstract Frontotemporal dementia is a heterogeneous neurodegenerative disorder characterized by neuronal loss in the frontal and temporal lobes. Despite progress in understanding which genes are associated with the aetiology of frontotemporal dementia, the biological basis of how mutations in these genes lead to cell loss in specific cortical regions remains unclear. In this work, we combined gene expression data for 16 772 genes from the Allen Institute for Brain Science atlas with brain maps of grey matter atrophy in symptomatic C9orf72, GRN and MAPT mutation carriers obtained from the Genetic Frontotemporal dementia Initiative study. No significant association was seen between C9orf72, GRN and MAPT expression and the atrophy patterns in the respective genetic groups. After adjusting for spatial autocorrelation, between 1000 and 5000 genes showed a negative or positive association with the atrophy pattern within each individual genetic group, with the most significantly associated genes being TREM2, SSBP3 and GPR158 (negative association in C9Orf72, GRN and MAPT respectively) and RELN, MXRA8 and LPA (positive association in C9Orf72, GRN and MAPT respectively). An overrepresentation analysis identified a negative association with genes involved in mitochondrial function, and a positive association with genes involved in vascular and glial cell function in each of the genetic groups. A set of 423 and 700 genes showed significant positive and negative association, respectively, with atrophy patterns in all three maps. The gene set with increased expression in spared cortical regions was enriched for neuronal and microglial genes, while the gene set with increased expression in atrophied regions was enriched for astrocyte and endothelial cell genes. Our analysis suggests that these cell types may play a more active role in the onset of neurodegeneration in frontotemporal dementia than previously assumed, and in the case of the positively associated cell marker genes, potentially through emergence of neurotoxic astrocytes and alteration in the blood–brain barrier, respectively.

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