Physcomitrium patens Infection by Colletotrichum gloeosporioides: Understanding the Fungal–Bryophyte Interaction by Microscopy, Phenomics and RNA Sequencing

Anthracnose caused by the hemibiotroph fungus Colletotrichum gloeosporioides is a devastating plant disease with an extensive impact on plant productivity. The process of colonization and disease progression of C. gloeosporioides has been studied in a number of angiosperm crops. To better understand the evolution of the plant response to pathogens, the study of this complex interaction has been extended to bryophytes. The model moss Physcomitrium patens Hedw. B&S (former Physcomitrella patens) is sensitive to known bacterial and fungal phytopathogens, including C. gloeosporioides, which cause infection and cell death. P. patens responses to these microorganisms resemble that of the angiosperms. However, the molecular events during the interaction of P. patens and C. gloeosporioides have not been explored. In this work, we present a comprehensive approach using microscopy, phenomics and RNA-seq analysis to explore the defense response of P. patens to C. gloeosporioides. Microscopy analysis showed that appressoria are already formed at 24 h after inoculation (hai) and tissue colonization and cell death occur at 24 hai and is massive at 48 hai. Consequently, the phenomics analysis showed progressing browning of moss tissues and impaired photosynthesis from 24 to 48 hai. The transcriptomic analysis revealed that more than 1200 P. patens genes were differentially expressed in response to Colletotrichum infection. The analysis of differentially expressed gene function showed that the C. gloeosporioides infection led to a transcription reprogramming in P. patens that upregulated the genes related to pathogen recognition, secondary metabolism, cell wall reinforcement and regulation of gene expression. In accordance with the observed phenomics results, some photosynthesis and chloroplast-related genes were repressed, indicating that, under attack, P. patens changes its transcription from primary metabolism to defend itself from the pathogen.

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

10.21203/rs.2.13011/v1 ◽

2019 ◽

Author(s):

Honglin Feng ◽

Xiao Guo ◽

Hongyan Sun ◽

Shuai Zhang ◽

Jinghui Xi ◽

...

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Flight Muscle ◽

Differentially Expressed Gene ◽

Instar Nymph ◽

Sitobion Avenae ◽

Differentially Expressed ◽

Terminal Deoxynucleotidyl Transferase ◽

Muscle Degeneration ◽

Flight Muscles

Abstract Objective Previous studies showed that flight muscles were degenerated 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 Wheat aphid starts to differentiate winged or wingless lines at the second instar nymph, determined at the third instar, and then fully developed at the fourth instar. After migration, the 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 gene, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration, during which endogenous proteins may be degraded to reallocate energy for reproduction.

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Decoding Psoriasis: Integrated Bioinformatics Approach to Understand Hub Genes and Involved Pathways

Current Pharmaceutical Design ◽

10.2174/1381612826666200311130133 ◽

2020 ◽

Vol 26 (29) ◽

pp. 3619-3630

Author(s):

Saumya Choudhary ◽

Dibyabhaba Pradhan ◽

Noor S. Khan ◽

Harpreet Singh ◽

George Thomas ◽

...

Keyword(s):

Gene Expression ◽

Differentially Expressed Gene ◽

Therapeutic Targets ◽

Interaction Network ◽

Gene Expression Omnibus ◽

Differentially Expressed ◽

Keratinocyte Differentiation ◽

Hub Genes ◽

Lesional Skin ◽

Ncbi Gene Expression Omnibus

Background: Psoriasis is a chronic immune mediated skin disorder with global prevalence of 0.2- 11.4%. Despite rare mortality, the severity of the disease could be understood by the accompanying comorbidities, that has even led to psychological problems among several patients. The cause and the disease mechanism still remain elusive. Objective: To identify potential therapeutic targets and affecting pathways for better insight of the disease pathogenesis. Method: The gene expression profile GSE13355 and GSE14905 were retrieved from NCBI, Gene Expression Omnibus database. The GEO profiles were integrated and the DEGs of lesional and non-lesional psoriasis skin were identified using the affy package in R software. The Kyoto Encyclopaedia of Genes and Genomes pathways of the DEGs were analyzed using clusterProfiler. Cytoscape, V3.7.1 was utilized to construct protein interaction network and analyze the interactome map of candidate proteins encoded in DEGs. Functionally relevant clusters were detected through Cytohubba and MCODE. Results: A total of 1013 genes were differentially expressed in lesional skin of which 557 were upregulated and 456 were downregulated. Seven dysregulated genes were extracted in non-lesional skin. The disease gene network of these DEGs revealed 75 newly identified differentially expressed gene that might have a role in development and progression of the disease. GO analysis revealed keratinocyte differentiation and positive regulation of cytokine production to be the most enriched biological process and molecular function. Cytokines -cytokine receptor was the most enriched pathways. Among 1013 identified DEGs in lesional group, 36 DEGs were found to have altered genetic signature including IL1B and STAT3 which are also reported as hub genes. CCNB1, CCNA2, CDK1, IL1B, CXCL8, MKI 67, ESR1, UBE2C, STAT1 and STAT3 were top 10 hub gene. Conclusion: The hub genes, genomic altered DEGs and other newly identified differentially dysregulated genes would improve our understanding of psoriasis pathogenesis, moreover, the hub genes could be explored as potential therapeutic targets for psoriasis.

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Identification of the Differentially Expressed Genes Involved in the Synergistic Neurotoxicity of an HIV Protease Inhibitor and Methamphetamine

Current HIV Research ◽

10.2174/1570162x17666190924200354 ◽

2019 ◽

Vol 17 (4) ◽

pp. 290-303

Author(s):

Sangsang Li ◽

Yanfei Li ◽

Bingpeng Deng ◽

Jie Yan ◽

Yong Wang

Keyword(s):

Protease Inhibitor ◽

Growth Inhibition ◽

Quantitative Polymerase Chain Reaction ◽

Differentially Expressed Gene ◽

Antiretroviral Drugs ◽

Differentially Expressed ◽

Hiv Protease ◽

Hiv Protease Inhibitor ◽

Dopaminergic Cells ◽

Immunodeficiency Syndrome

Background: The abuse of psychostimulants such as methamphetamine (METH) is common in human immunodeficiency virus (HIV)-infected individuals. Acquired immunodeficiency syndrome (AIDS) patients taking METH and antiretroviral drugs could suffer severe neurologic damage and cognitive impairment. Objective: To reveal the underlying neuropathologic mechanisms of an HIV protease inhibitor (PI) combined with METH, growth-inhibition tests of dopaminergic cells and RNA sequencing were performed. Methods: A combination of METH and PI caused more growth inhibition of dopaminergic cells than METH alone or a PI alone. Furthermore, we identified differentially expressed gene (DEG) patterns in the METH vs. untreated cells (1161 genes), PI vs. untreated cells (16 genes), METH-PI vs. PI (3959 genes), and METH-PI vs. METH groups (14 genes). Results: The DEGs in the METH-PI co-treatment group were verified in the brains of a mouse model using quantitative polymerase chain reaction and were involved mostly in the regulatory functions of cell proliferation and inflammation. Conclusion: Such identification of key regulatory genes could facilitate the study of their neuroprotective potential in the users of METH and PIs.

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Gene Set Correlation Analysis and Visualization Using Gene Expression Data

Current Bioinformatics ◽

10.2174/1574893615999200629124444 ◽

2020 ◽

Vol 15 ◽

Author(s):

Chen-An Tsai ◽

James J. Chen

Keyword(s):

Gene Expression ◽

Correlation Analysis ◽

Gene Expression Data ◽

Differentially Expressed Gene ◽

Differentially Expressed ◽

Superior Performance ◽

Expression Data ◽

Gene Set ◽

Gene Sets ◽

Set Correlation

Background: Gene set enrichment analyses (GSEA) provide a useful and powerful approach to identify differentially expressed gene sets with prior biological knowledge. Several GSEA algorithms have been proposed to perform enrichment analyses on groups of genes. However, many of these algorithms have focused on identification of differentially expressed gene sets in a given phenotype. Objective: In this paper, we propose a gene set analytic framework, Gene Set Correlation Analysis (GSCoA), that simultaneously measures within and between gene sets variation to identify sets of genes enriched for differential expression and highly co-related pathways. Methods: We apply co-inertia analysis to the comparisons of cross-gene sets in gene expression data to measure the costructure of expression profiles in pairs of gene sets. Co-inertia analysis (CIA) is one multivariate method to identify trends or co-relationships in multiple datasets, which contain the same samples. The objective of CIA is to seek ordinations (dimension reduction diagrams) of two gene sets such that the square covariance between the projections of the gene sets on successive axes is maximized. Simulation studies illustrate that CIA offers superior performance in identifying corelationships between gene sets in all simulation settings when compared to correlation-based gene set methods. Result and Conclusion: We also combine between-gene set CIA and GSEA to discover the relationships between gene sets significantly associated with phenotypes. In addition, we provide a graphical technique for visualizing and simultaneously exploring the associations of between and within gene sets and their interaction and network. We then demonstrate integration of within and between gene sets variation using CIA and GSEA, applied to the p53 gene expression data using the c2 curated gene sets. Ultimately, the GSCoA approach provides an attractive tool for identification and visualization of novel associations between pairs of gene sets by integrating co-relationships between gene sets into gene set analysis.

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Lipidomics profiling of goose granulosa cell model of stearoyl-CoA desaturase function identifies a pattern of lipid droplets associated with follicle development

Cell & Bioscience ◽

10.1186/s13578-021-00604-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Xin Yuan ◽

Shenqiang Hu ◽

Liang Li ◽

Chunchun Han ◽

Hehe Liu ◽

...

Keyword(s):

Differentially Expressed Genes ◽

Lipid Droplets ◽

Cell Model ◽

Enrichment Analysis ◽

Differentially Expressed ◽

Pathway Enrichment Analysis ◽

Follicle Development ◽

Microscopy Analysis ◽

Stearoyl Coa Desaturase ◽

Underlying Mechanisms

Abstract Background Despite their important functions and nearly ubiquitous presence in cells, an understanding of the biology of intracellular lipid droplets (LDs) in goose follicle development remains limited. An integrated study of lipidomic and transcriptomic analyses was performed in a cellular model of stearoyl-CoA desaturase (SCD) function, to determine the effects of intracellular LDs on follicle development in geese. Results Numerous internalized LDs, which were generally spherical in shape, were dispersed throughout the cytoplasm of granulosa cells (GCs), as determined using confocal microscopy analysis, with altered SCD expression affecting LD content. GC lipidomic profiling showed that the majority of the differentially abundant lipid classes were glycerophospholipids, including PA, PC, PE, PG, PI, and PS, and glycerolipids, including DG and TG, which enriched glycerophospholipid, sphingolipid, and glycerolipid metabolisms. Furthermore, transcriptomics identified differentially expressed genes (DEGs), some of which were assigned to lipid-related Gene Ontology slim terms. More DEGs were assigned in the SCD-knockdown group than in the SCD-overexpression group. Integration of the significant differentially expressed genes and lipids based on pathway enrichment analysis identified potentially targetable pathways related to glycerolipid/glycerophospholipid metabolism. Conclusions This study demonstrated the importance of lipids in understanding follicle development, thus providing a potential foundation to decipher the underlying mechanisms of lipid-mediated follicle development.

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571 Molecular events during cold stress induced cell-death on multidrug resistant leukemic cells

European Journal of Cancer Supplements ◽

10.1016/s1359-6349(10)71372-0 ◽

2010 ◽

Vol 8 (5) ◽

pp. 145-146

Author(s):

D. Cerezo ◽

A.J. Ruiz-Alcaraz ◽

M. Lencina ◽

C. Bernal ◽

M. Cánovas ◽

...

Keyword(s):

Cell Death ◽

Cold Stress ◽

Multidrug Resistant ◽

Leukemic Cells ◽

Molecular Events

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Human HtrA, an Evolutionarily Conserved Serine Protease Identified as a Differentially Expressed Gene Product in Osteoarthritic Cartilage

Journal of Biological Chemistry ◽

10.1074/jbc.273.51.34406 ◽

1998 ◽

Vol 273 (51) ◽

pp. 34406-34412 ◽

Cited By ~ 145

Author(s):

Shou-Ih Hu ◽

Marc Carozza ◽

Melissa Klein ◽

Pascale Nantermet ◽

Daniel Luk ◽

...

Keyword(s):

Serine Protease ◽

Gene Product ◽

Differentially Expressed Gene ◽

Differentially Expressed ◽

Osteoarthritic Cartilage ◽

Evolutionarily Conserved

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Protein synthesis persists during necrotic cell death

The Journal of Cell Biology ◽

10.1083/jcb.200407162 ◽

2005 ◽

Vol 168 (4) ◽

pp. 545-551 ◽

Cited By ~ 49

Author(s):

Xavier Saelens ◽

Nele Festjens ◽

Eef Parthoens ◽

Isabel Vanoverberghe ◽

Michael Kalai ◽

...

Keyword(s):

Cell Death ◽

Protein Synthesis ◽

De Novo ◽

Translation Initiation Factor ◽

Initiation Factor ◽

Necrotic Cell Death ◽

Necrotic Cell ◽

Proteolytic Activation ◽

Double Stranded Rna ◽

Molecular Events

Cell death is an intrinsic part of metazoan development and mammalian immune regulation. Whereas the molecular events orchestrating apoptosis have been characterized extensively, little is known about the biochemistry of necrotic cell death. Here, we show that, in contrast to apoptosis, the induction of necrosis does not lead to the shut down of protein synthesis. The rapid drop in protein synthesis observed in apoptosis correlates with caspase-dependent breakdown of eukaryotic translation initiation factor (eIF) 4G, activation of the double-stranded RNA-activated protein kinase PKR, and phosphorylation of its substrate eIF2-α. In necrosis induced by tumor necrosis factor, double-stranded RNA, or viral infection, de novo protein synthesis persists and 28S ribosomal RNA fragmentation, eIF2-α phosphorylation, and proteolytic activation of PKR are absent. Collectively, these results show that, in contrast to apoptotic cells, necrotic dying cells retain the opportunity to synthesize proteins.

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