This SuperSeries is composed of the SubSeries listed below.
MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation.
Specimen part
View SamplesWe identified microRNA-188 differentially expressed in the BMSCs of aged and young mice and influenced on BMSCs differentiation with ageing.
MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation.
Specimen part
View SamplesWe identified microRNA-188 differentially expressed in the BMSCs of aged and young mice and influented on BMSCs differentiation with ageing.
MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation.
Specimen part
View SamplesIn this data set, we reported for the first time that huanglongbing disease (HLB) induces major changes in the expression of global genes in flavedo, vascular and juice vesicle tissues of citrus fruit.
Gene expression in Citrus sinensis fruit tissues harvested from huanglongbing-infected trees: comparison with girdled fruit.
Specimen part
View SamplesTo understand the differentiation of effector Tregs in more detail, we have performed transcriptional profiling of central Tregs and effector Tregs, based on Blimp1 expression. We performed RNA-sequencing of Foxp3+ regulatory T cells, comparing Blimp1/GFP+ and Blimp1/GFP- cells Overall design: Three biologically independent samples for each condition were sequenced (condition 1: CD4+ CD25high Blimp1/GFP+; condition 2: CD4+ CD25high Blimp1/GFP-); cells were sorted from pooled spleens and lymphnodes of Blimp1/GFP reporter mice
The transcriptional regulators IRF4, BATF and IL-33 orchestrate development and maintenance of adipose tissue-resident regulatory T cells.
No sample metadata fields
View SamplesIn order to study the importance of HSFA1 in thermotolerance in Arabidopsis, we generated the HSFA1a, b, d and e quadruple mutant (QK). QK is very sensitive to heat. Therefore, we used microarray to study how many genes regulated by HSFA1 after heat shock.
The role of class A1 heat shock factors (HSFA1s) in response to heat and other stresses in Arabidopsis.
Age, Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The transcription factor Foxo1 controls central-memory CD8+ T cell responses to infection.
Specimen part
View SamplesTristetraprolin is a vertebrate CCCH tandem zinc finger protein that can bind to and destabilize certain mRNAs containing AU-rich element binding sites. zfs1 is the single gene in the fission yeast, Schizosaccharomyces pombe, that encodes a protein containing the critical features of the tristetraprolin zinc finger domain. zfs1 has been linked to pheromone signal transduction control and to the coordination of mitosis, but no biological function has been ascribed to the zfs1 protein. Through a functional genomics approach we compared transcript levels in wild-type and zfs1-deficient S. pombe strains; those elevated in the zfs1-deficient strain were examined for the presence of potential tristetraprolin-like binding sites. One such potential target transcript was encoded by arz1, a gene encoding a protein of unknown function that contains armadillo repeats. arz1 mRNA decay was inhibited in the zfs1-deficient strain when it was expressed under the control of a thiamine-repressible promoter. Mutations within one AU-rich element present in the arz1 3-untranslated region protected this transcript from zfs1-promoted decay, whereas mutating another potential binding site had no effect. Binding assays confirmed a direct interaction between zfs1 and arz1 mRNA-based probes; this interaction was eliminated when key residues were mutated in either zfs1 zinc finger. zfs1 and its targets in S. pombe represent a useful model system for studies of zinc finger protein/AU-rich element interactions that result in mRNA decay.
Characterization of zfs1 as an mRNA-binding and -destabilizing protein in Schizosaccharomyces pombe.
No sample metadata fields
View SamplesRegulatory T cells (Tregs) expressing the transcription factor Foxp3 have a pivotal role in maintaining immunological self-tolerance1-5; yet, excessive Treg activities suppress anti-tumor immune responses6-8. Compared to resting phenotype Tregs (rTregs) in the secondary lymphoid organs, Tregs in non-lymphoid tissues including solid tumors exhibit an activated Treg (aTreg) phenotype9-11. However, aTreg function and whether its generation can be manipulated to promote tumor immunity without evoking autoimmunity are largely unexplored. Here we show that the transcription factor Foxo1, previously demonstrated to promote Treg suppression of lymphoproliferative diseases12,13, has an unexpected function in inhibiting aTreg-mediated immune tolerance. We found that aTregs turned over at a slower rate than rTregs, but were not locally maintained in tissues. Transcriptome analysis revealed that aTreg differentiation was associated with repression of Foxo1-dependent gene transcription, concomitant with reduced Foxo1 expression, cytoplasmic Foxo1 localization, and enhanced Foxo1 phosphorylation at sites of the Akt kinase. Treg-specific expression of an Akt-insensitive Foxo1 mutant prevented downregulation of lymphoid organ homing molecules, and impeded Treg homing to non-lymphoid organs, causing CD8+ T cell-mediated autoimmune diseases. Compared to Tregs from healthy tissues, tumor-infiltrating Tregs downregulated Foxo1 target genes more substantially. Expression of the Foxo1 mutant at a lower dose was sufficient to deplete tumor-associated Tregs, activate effector CD8+ T cells, and inhibit tumor growth without inflicting autoimmunity. Thus, Foxo1 inactivation is essential for the migration of aTregs that have a crucial function in suppressing CD8+ T cell responses; and the Foxo signaling pathway in Tregs can be titrated to preferentially break tumor immune tolerance. Overall design: Transcriptome of splenic rTreg (CD4+Foxp3+CD62LhiCD44lo) and aTreg (CD4+Foxp3+CD62LhiCD44lo) were compared. Duplicates from biologically independent animials were used.
Graded Foxo1 activity in Treg cells differentiates tumour immunity from spontaneous autoimmunity.
Specimen part, Subject
View SamplesMemory T cells provide immunity against pathogen reinvasion, but mechanisms of their long-term maintenance is unclear. Here we show that mice with the deletion of the transcription factor Foxo1 in activated CD8+ T cells had defective secondary but not primary responses to Listeria monocytogenes infection. Compared to short-lived effector T cells, memory precursor effector T cells expressed higher amounts of Foxo1 that promoted their generation and maintenance. Gene expression profiling and chromatin immunoprecipitation sequencing experiments revealed the chemokine receptor CCR7 and the transcription factor TCF1 as novel Foxo1-bound target genes with critical functions in memory T cell trafficking and transcriptional regulation. These findings demonstrate that Foxo1 is selectively incorporated into the genetic program that regulates memory but not effector CD8+ T cell responses to infection.
The transcription factor Foxo1 controls central-memory CD8+ T cell responses to infection.
Specimen part
View Samples