This SuperSeries is composed of the SubSeries listed below.
Genome-wide DNA methylation and gene expression analyses of monozygotic twins discordant for intelligence levels.
Specimen part
View SamplesHuman intelligence demonstrates one of the highest heritabilities among human quantitative traits. Phenotypically discordant monozygotic twins provide a way to identify loci responsible for normal-range intelligence.
Genome-wide DNA methylation and gene expression analyses of monozygotic twins discordant for intelligence levels.
Specimen part
View SamplesTOLS2 regulates lateral root initiation in Arabidopsis thaliana.
No associated publication
Specimen part
View SamplesLateral roots (LRs) are formed post-embryonically and contribute to root architecture formation in vascular plants. LATERAL ORGAN BOUNDARIES-DOMAIN 16 (LBD16) is a key transcription factor to initiate LR formation functioning redundantly with related LBD members. To identify primary downstream targets of LBD16, we engineered a transgenic line with inducible LBD16 activity by expressing a fusion protein of LBD16 and rat glucocorticoid receptor (GR) under the regulation of its own regulatory region (gLBD16-GR) in the lbd16-1 lbd18-1 lbd33-1 mutant. Here we identified primary response genes of LBD16 from transcriptome analysis.
No associated publication
Specimen part, Treatment
View SamplesLateral roots (LRs) are formed post-embryonically and contribute to root architecture formation in vascular plants. LATERAL ORGAN BOUNDARIES-DOMAIN 16 (LBD16) is a key transcription factor to initiate LR formation. LBD16 functions downstream of AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19, and overexpression of LBD16 partially restores LR formation in the absence of ARF7 and ARF19. To identify downstream targets of LBD16, we engineered a transgenic line with inducible LBD16 activity by overexpressing a fusion protein of LBD16 and rat glucocorticoid receptor (GR) in arf7 arf19 mutant. Here we identified primary response genes of LBD16 from transcriptome analysis of 35Spro:LBD16:GR arf7 arf19 line.
No associated publication
Specimen part, Treatment
View SamplesXPA is required for Nucleotide Excision Repair system, which could function to repair DNA damage induced by the UV. UV damage on the genomic DNA cannot be removed, thus persistence of damage could affect the transcriptional machinary.
Mitotic genes are transcriptionally upregulated in the fibroblast irradiated with very low doses of UV-C.
Specimen part, Disease
View SamplesDeregulated retinal angiogenesis directly cause vision loss in many ocular diseases, such as diabetic retinopathy and retinopathy of prematurity. To identify endothelial-specific genes expressed in angiogenic retinal vessels, we purified genetically labeled endothelial cells from Tie2-GFP transgenic mice and performed gene expression profiling using DNA microarray. To find out genes associated with angiogenesis, comparisons of microarray data were carried out between GFP-negative non-endothelial retinal cells and GFP-positive retinal endothelial cells in angiogenic P8 retina.
Sema3E-PlexinD1 signaling selectively suppresses disoriented angiogenesis in ischemic retinopathy in mice.
Specimen part
View SamplesPericytes confer vascular stability in the retina, and the loss of pericytes can cause the blood-retina barrier breakdown seen in diabetic retinopathy. To identify endothelial-specific genes expressed in pericyte-deprived retinal vessels, we purified genetically labeled endothelial cells from Tie2-GFP transgenic mice treated with neutralizing antibody against PDGFRb (APB5) and performed gene expression profiling using DNA microarray. To find out endothelial-specific genes associated with the loss of pericyte coverage, the comparison of microarray data was carried out between retinal endothelial cells (data from GSE27238) and APB5-treated retinal endothelial cells.
Sustained inflammation after pericyte depletion induces irreversible blood-retina barrier breakdown.
Specimen part
View SamplesDecoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor (TNFR) superfamily, competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT, and TL1A. DcR3 was recently reported not only to act as a decoy receptor for these TNFRs but also to play a role as a ligand for the pathogenesis of RA.
Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts.
Specimen part, Race
View SamplesTNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFB by binding to its specific receptor death receptor 3 (DR3). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble TL1A in addition to Fas-ligand (FasL) and LIGHT and inhibits the signaling of TL1A via DR3. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNF or IL-1 inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. Therefore, TL1A-DcR3/DR3 signaling may be involved in the pathogenesis of RA by modulating apoptosis and proliferation of RA-FLS.
No associated publication
Specimen part, Treatment, Race
View Samples