To understand plant adaptation to heat stress, gene expression profiles of Arabidopsis leaves under heat stress, during recovery and control condition were obtained using microarray. Microarray data listed responsible candidate genes for glycerolipid metabolism.
Landscape of the lipidome and transcriptome under heat stress in Arabidopsis thaliana.
Age, Specimen part
View SamplesPRR5 transcription factor acts in the circadian clock system. To elucidate regulated genes by PRR5, Chimeric protein PRR5-VP, which activates direct target genes of PRR5, was over-expressed in Col-0. Microarray analsysis was performed using these plants with Affymetrix ATH1 genechip.
Transcriptional repressor PRR5 directly regulates clock-output pathways.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcription factor Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate.
Specimen part, Treatment
View SamplesRecent studies have identified Zeb2 as a transcription factor important for the final maturation of natural killer cells and effector CD8+ T cells. We show that Zeb2 is required for the development of two myeloid cell types, the monocyte and the plasmacytoid dendritic cell, and clarify that this factor is not required for the development of classical dendritic cells.
Transcription factor Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate.
Specimen part, Treatment
View SamplesRecent studies have identified Zeb2 as a transcription factor important for the final maturation of natural killer cells and effector CD8+ T cells. We show that Zeb2 is required for the development of two myeloid cell types, the monocyte and the plasmacytoid dendritic cell, and clarify that this factor is not required for the development of classical dendritic cells.
Transcription factor Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate.
Specimen part
View SamplesBy using a genetically accurate mouse model, we demonstrate that endogenous expression of oncogenic N-RasG12D and Tet2 haploinsufficiency collaborate to accelerate CMML development in mice. Gene expression was compared across all genotypes (WT, Tet2+/-, NrasG12D/+ and double mutants) in bone marrow-derived hematopoietic stem cells (CD150+CD48-Lin-Sca1+cKit+) using RNA-seq. N-RasG12D and Tet2 haploinsufficiency cooperate to induce both unique and overlapping effects on HSC gene expression programs. Overall design: Gene expression profiling in FACS-sorted SLAM HSCs from 10-12 week old wild type control (n=3), NrasG12D/+ single mutant (n=3), Tet2+/- single mutant (n=3) and NrasG12D/+;Tet2+/- double mutant (n=3) mice.
Oncogenic N-Ras and Tet2 haploinsufficiency collaborate to dysregulate hematopoietic stem and progenitor cells.
Specimen part, Cell line, Subject
View SamplesTo identify genes that regulate root development in a hydrogen peroxide devendent manner, we performed a time course microarray analysis of root treated with 1mM H2O2.
MYB30 links ROS signaling, root cell elongation, and plant immune responses.
Age, Specimen part, Time
View SamplesUsing wild type and Ash1l deltaSET mutant embryonic stem cells, here we report differences of gene expression pattern under undifferentiated state and differentiated state. Interestingly, gene expression changes are frequently observed in a subset of gene group that is regulated by Polycomb group proteins. Overall design: Examination of 2 cell types in 2 different conditions.
Ash1l methylates Lys36 of histone H3 independently of transcriptional elongation to counteract polycomb silencing.
Cell line, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dual-mode modulation of Smad signaling by Smad-interacting protein Sip1 is required for myelination in the central nervous system.
Specimen part
View SamplesMyelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and -catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair.
Dual-mode modulation of Smad signaling by Smad-interacting protein Sip1 is required for myelination in the central nervous system.
Specimen part
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