Interaction between the host and invading pathogen determines the fate of both organisms during the infectious state. The host is equipped with a battery of immune reactions, while the pathogen displays a variety of mechanisms to compromise host immunity. Although bacteria alter their pattern of gene expression when they enter host organisms, studies to elucidate the mechanism behind this are only in their infancy. In the present study, we examined the possibility that host immune proteins directly participate in the change of gene expression in bacteria. To this end, Escherichia coli was treated with a mixture of the extracellular region of membrane-bound peptidoglycan recognition protein LC (PGRP-LC) and the antimicrobial peptide attacin of Drosophila, and subsequently subjected to DNA microarray analysis for the repertoire of mRNA. We identified nearly 200 genes whose mRNA increased after the treatment, and at least four of them were induced in response to PGRP-LC. One such gene, lipoprotein-encoding nlpI, showed a transient increase of its mRNA level in adult flies depending on PGRP-LC, and NlpI-lacking E. coli had a smaller pathogenic effect with lowered growth/viability than the parental strain in adult flies. These results suggest that a host immune receptor triggers a change of gene expression in bacteria simultaneously to their recognition of the invader and induction of immune responses.
Peptidoglycan recognition protein-triggered induction of Escherichia coli gene in Drosophila melanogaster.
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View SamplesGene expression was examined in granulosa cells and oocytes in various stage of follicle and in vitro grown oocytes and granulosa cells complexes in sus scrofa.
Gene expression patterns in granulosa cells and oocytes at various stages of follicle development as well as in in vitro grown oocyte-and-granulosa cell complexes.
Specimen part
View SamplesPurpose: The goals of this study are to elucidate the influence of integrin ß3 signaling on STAT1-dependnet gene expression in IFN?-treated HSCs. Methods: Wild type (WT) HSCs were cultured with or without IFN? and/or VN in the presence of stem cell factor (SCF) plus thrombopoietin (TPO). Subsequently, cultured HSC fraction (CD48- c-kit+ Sca-1+ Lineage-) were sorted, followed by mRNA sequence using Ion Proton (n>4). Moreover, to extract genes whose expression were changed via STAT1 in the presence of IFN?, mRNA profiles of STAT1-/- HSCs treated with or without IFN? were also generated by the same way. The sequence reads that passed quality filters were analyzed by CLC genomic workbench. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm10) with CLC genomic workbench. Indeed, hierarchical clustering analysis showed that IFN?-treated STAT1-/- HSCs was categorized to the group including Wt HSCs cultured in the absence of IFN? rather than HSCs treated with IFN?. Furthermore, gene set enrichment analysis (GSEA) showed that STAT1-dependent upregulated gene sets were significantly enriched within genes whose expression was enhanced in HSCs treated with VN and IFN?. In contrast, integrin ß3 signaling in the absence of IFN? appears to not influence the expression of IFN?/STAT1-dependent genes, as evidenced by the observation that VN treatment was statistically and significantly independent of the enrichment of gene sets that were both up-regulated by STAT1 Conclusions: Our study represents that STAT1 plays a central role in IFN?-mediated HSC responses and integrin ß3 signaling in HSCs promotes STAT1-dependent gene expression in the presence of IFN?. Overall design: After HSCs derived from wild type (WT) and STAT1-/- mice were treated with IFNg and/or vitronectin for 5 days, mRNA profiles were generated by deep sequencing using Ion Proton system (n>4).
Integrin αvβ3 enhances the suppressive effect of interferon-γ on hematopoietic stem cells.
Specimen part, Cell line, Subject
View SamplesThe phagocytic elimination of cells undergoing apoptosis is an evolutionarily conserved innate immune mechanism for eliminating unnecessary cells. Previous studies showed an increase in the level of engulfment receptors in phagocytes after the phagocytosis of apoptotic cells, which leads to the enhancement of their phagocytic activity. However, precise mechanisms underlying this phenomenon require further clarification. We found that the pre-incubation of a Drosophila phagocyte cell line with the fragments of apoptotic cells enhanced the subsequent phagocytosis of apoptotic cells, accompanied by an augmented expression of the engulfment receptors Draper and integrin PS3. The DNA-binding activity of the transcription repressor Tailless was transiently raised in those phagocytes, depending on two partially overlapping signal-transduction pathways for the induction of phagocytosis as well as the occurrence of engulfment. The RNAi knockdown of tailless in phagocytes abrogated the enhancement of both phagocytosis and engulfment receptor expression. Furthermore, the hemocyte-specific RNAi of tailless reduced apoptotic cell clearance in Drosophila embryos. Taken together, we propose the following mechanism for the activation of Drosophila phagocytes after an encounter with apoptotic cells: two partially overlapping signaltransduction pathways for phagocytosis are initiated; transcription repressor Tailless is activated; expression of engulfment receptors is stimulated; and phagocytic activity is enhanced. This phenomenon most likely ensures the phagocytic elimination of apoptotic cells that stimulated phagocytes find thereafter and is thus considered as a mechanism to prime phagocytes in innate immunity.
Signaling pathway for phagocyte priming upon encounter with apoptotic cells.
Cell line, Treatment, Time
View SamplesThe character of the earliest cardiac precursor cells remains largely unknown. To elucidate this further, we constructed single cell cDNAs from the mouse embryonic cardiac precurcsor cells of the early allantoic bud stage and the early headfold stage, and subjected them to deep sequencing. Overall design: The most anterior part of the embryos where cardiac precursor cells exist was digested by trypsin to separate into single cells. After a cell was transferred into a reaction tube, single cell cDNAs were constructed as PCR amplicons. cDNAs of cardiac precursor cells were identified by PCR of marker genes.
Single-Cell Expression Profiling Reveals a Dynamic State of Cardiac Precursor Cells in the Early Mouse Embryo.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Methionine metabolism regulates maintenance and differentiation of human pluripotent stem cells.
Specimen part, Cell line
View SamplesIn undifferentiated human ES cells, 5hr Met deprivation (delta Met) led to decreased proliferation, and prolonged 24hr Met deprivation resulted in G0-G1 phase cell cycle arrest, which then led to apoptosis.
Methionine metabolism regulates maintenance and differentiation of human pluripotent stem cells.
Specimen part, Cell line
View SamplesIn undifferentiated human ES cells, 48hr Leucine deprivation (delta Leu) or Lysine deprivation (delta Lys) led to apoptosis.
Methionine metabolism regulates maintenance and differentiation of human pluripotent stem cells.
Specimen part, Cell line
View SamplesAnalysis of HEK293T cells overexpressing ZAPS (zinc finger antiviral protein, short form; NP_078901), which is a member of the PARP (poly (ADP-ribose) polymerase)-superfamily. Results of gene profiles provide insight into the role of ZAPS in innate immunity.
ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses.
Specimen part, Cell line
View SamplesWe compared the expression among three lines, Col, C24, and their hybrids at 10 days after sowing (DAS).
Heterosis of Arabidopsis hybrids between C24 and Col is associated with increased photosynthesis capacity.
Specimen part
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