To identify and characterize genes required for tissue-specific phytochrome responses during hypocotyl development in far-red-light grown bvr lines, we performed gene transcriptional profiling using bvr lines with mesophyll-specific phytochrome inactivation (cab3: :pBVR2). We identified several candidate genes whose expression is significantly altered in lines with mesophyll tissue-specific BVR expression (Cab3::pBVR2), compared to constitutive phytochrome inactivation lines, i.e. 35S-driven BVR lines (35S::pBVR3). No-0 is used as wild-type (WT)
Downstream effectors of light- and phytochrome-dependent regulation of hypocotyl elongation in Arabidopsis thaliana.
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The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle.
Cell line, Time
View SamplesBTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we performed knock-down of BACH1 in HEK 293T cells using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays.
The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle.
Cell line, Time
View SamplesWe have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii. Overall design: RNA-seq analysis of blood samples obtained from mice infected with Plasmodium chabaudi chabaudi, murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei.
Transcriptional profiling unveils type I and II interferon networks in blood and tissues across diseases.
Specimen part, Subject
View SamplesWe have performed modular analyses to decipher the global transcriptional response and capture a breadth of distinct immune responses in the lungs and blood of mice infected or challenged with a broad spectrum of infectious pathogens, including parasites (Toxoplasma gondii), bacteria (Burkholderia pseudomallei), viruses (Influenza A virus and Respiratory Syncytial virus (RSV)) and fungi (Candida albicans), or allergens (House dust mite (HDM), systemic and intra-nasal challenge). In a distinct set of infectious diseases, we tested the blood modular transcriptional signatures in mice infected with Plasmodium chabaudi chabaudi (malaria), murine cytomegalovirus (MCMV), Listeria monocytogenes and chronic Burkholderia pseudomallei. We also investigated the transcriptional profiles of sorted CD4 T cells (total CD4+, CD4+ CD44 high and CD4+ CD44 low) from lung and blood samples from mice challenged with HDM allergen. Moreover, we used mice deficient in either Ifnar or Ifngr, or both, to reveal the individual roles of each pathway in controlling disease in mice infected with Toxoplasma gondii. Overall design: RNA-seq analysis of sorted CD4 T cells (total CD4+, CD4+CD44high and CD4+CD44low) from lung and blood samples obtained from mice challenged systemically with House dust mite (HDM) allergy.
Transcriptional profiling unveils type I and II interferon networks in blood and tissues across diseases.
Specimen part, Subject
View SamplesMutation of marA, rob, and soxS causes a clinical strain of E.coli to be attenuated at d3 post-infection in a mouse model of pyelonephritis, here we extract RNA at d2 post infection to analyze transcriptional differences between the two strains.
SoxS increases the expression of the zinc uptake system ZnuACB in an Escherichia coli murine pyelonephritis model.
Specimen part
View SamplesF4/80+ macrophages treated with TGFb2 are potently tolerogenic. Our understanding of the molecular mechanisms mediating the development of these tolerogenic properties is incomplete.
FcγRI is required for TGFβ2-treated macrophage-induced tolerance.
Sex, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of the cortical neurons that mediate antidepressant responses.
Specimen part, Treatment
View SamplesMolecular phenotyping of cell types and neural circuits underlying pathological neuropsychiatric conditions and their responses to therapy provides one avenue for the development of more specific and effective treatments. In this study, we identify a cell population in the cerebral cortex that shows robust and specific molecular adaptations following long-term SSRI treatment.
Identification of the cortical neurons that mediate antidepressant responses.
Specimen part, Treatment
View SamplesMolecular phenotyping of cell types and neural circuits underlying pathological neuropsychiatric conditions and their responses to therapy provides one avenue for the development of more specific and effective treatments. In this study, we identify a cell population in the cerebral cortex that shows robust and specific molecular adaptations following long-term SSRI treatment.
Identification of the cortical neurons that mediate antidepressant responses.
Specimen part, Treatment
View Samples