Keeping imbibed seeds at low temperatures for a certain period, so called seed vernalization (SV) treatment, promotes seed germination and subsequent flowering in various plants. Vernalization-promoting flowering requires GSH. However, the expression patterns analyzed by GeneChip arrays showed that increased GSH biosynthesis partially mimics SV treatment in Arabidopsis thaliana. SV treatment (keeping imbibed seeds at 4C for 24 h) induced a specific pattern of gene expression and promoted subsequent flowering in wild-type plants. A similar pattern was observed at 22C in transgenic plants (35S-GSH1 plants) overexpressing the -glutamylcysteine synthetase gene GSH1, coding an enzyme limiting GSH biosynthesis, under the control of the cauliflower mosaic virus 35S promoter. This pattern was strengthened at 4C but flowering was less responsive to SV treatment. There was a difference in the transcript behaviour of the flowering repressor FLC between wild-type and 35S-GSH1 plants. Unlike other genes responsive to SV treatment, SV-dependent decrease in FLC in wild-type plants was reversed in 35S-GSH1 plants. SV treatment increased GSSG level in wild-type seeds, whereas GSSG level was high in 35S-GSH1 plants, even at a non-vernalizing temperature. Taking into consideration that low temperatures stimulate GSH biosynthesis and bring about oxidative stress, GSSG is considered to trigger low temperature response, but enhanced GSH synthesis was not enough for mimicking SV treatment. To complete it, it essentially required the cellular redox retransition from the oxidized to the reduced state that is observed after the seed vernalization treatment.
Overexpression of GSH1 gene mimics transcriptional response to low temperature during seed vernalization treatment of Arabidopsis.
Specimen part
View SamplesTransient mitochondrial stress can promote beneficial physiological responses and longevity, termed "mitohormesis." To interrogate mitohormetic pathways in mammals, we generated mice in which mitochondrial superoxide dismutase 2 (SOD2) can be knocked-down in an inducible and reversible manner (iSOD2-KD). Depleting SOD2 only during embryonic development did not cause post-natal lethality, allowing us to probe adaptive responses to mitochondrial oxidant stress in adult mice. Liver from adapted mice had increased mitochondrial biogenesis and antioxidant gene expression and fewer reactive oxygen species. Gene expression analysis implicated non- canonical activation of the Nrf2 antioxidant and PPAR-PGC-1 mitochondrial signaling pathways in this response. Transient SOD2 knock-down in embryonic fibroblasts from iSOD2-KD mice also resulted in adaptive mitochondrial changes, enhanced antioxidant capacity, and resistance to a subsequent oxidant challenge. We propose that mitohormesis in response to mitochondrial oxidative stress in mice involves sustained basal activation of mitochondrial and antioxidant signaling pathways to establish a heightened antioxidant state.
No associated publication
Sex, Age, Specimen part
View SamplesAims to find out differential expression genes (DEGs)in RAW264.7 cells during infection by Burkholderia pseudomallei infection
No associated publication
None
Sex, Specimen part, Cell line, Treatment
View SamplesDuring the pathogenesis of virus disease, lots of changes occur in plant hosts including the altered gene expression profiles. Rice stripe virus (RSV) is the type member of Tenuivirus, transmitted by Laodelphax striatellus in a circulative propagative man
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View SamplesTotal 23 samples were derived from [1] HUVEC treated in the absence (0h) or presence of hypoxia (1, 2, 4, 8, 12, and 24 hrs) to determine hypoxia-regulated gene in endothelial cells, [2] control siRNA or HIF1 siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [3] control siRNA or KDM3A siRNA transfected HUVEC cells treated in the absence or presence of hypoxia, [4] ChIP-seq data for HIF1 binding sites and histone modifications under normoxia and hypoxia in endothelial cells.
Dynamic change of chromatin conformation in response to hypoxia enhances the expression of GLUT3 (SLC2A3) by cooperative interaction of hypoxia-inducible factor 1 and KDM3A.
Cell line, Treatment
View SamplesIn order to clarify the downstream target genes of SPAG4, we performed knockdown of SPAG4 using siRNA both under normoxia and hypoxia.
Sperm-associated antigen 4, a novel hypoxia-inducible factor 1 target, regulates cytokinesis, and its expression correlates with the prognosis of renal cell carcinoma.
Cell line
View SamplesWe generated three kinds of genetically identical mouse reprogrammed cells: induced pluripotent stem cells (iPSCs), nuclear transfer embryonic stem cells (ntESCs) and iPSC-nt-ESCs that are established after successively reprogramming of iPSCs by nuclear transfer (NT). NtESCs show better developmental potential than iPSCs, whereas iPSC-nt-ESCs display worse developmental potential than iPSCs.
No associated publication
Sex, Specimen part, Cell line
View SamplesNEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer.
NEDD9 promotes lung cancer metastasis through epithelial-mesenchymal transition.
Specimen part, Cell line
View SamplesThe intestinal epithelial barrier plays a critical role in the mucosal immunity. However, it remains largely unknown how the epithelial barrier is maintained after damage. Here we show that FGF2 synergizes with IL-17A to induce genes for repairing of damaged epithelium. Deficiency of FGF2 or IL-17A resulted in impaired epithelial proliferation, increased pro-inflammatory microbiota outgrowth, and consequently worse pathology in a DSS-induced colitis model.
Growth Factor FGF2 Cooperates with Interleukin-17 to Repair Intestinal Epithelial Damage.
Specimen part
View SamplesBACKGROUND: The vast majority of thoracic aortic aneurysms (TAAs) are observed either together with a bicuspid aortic valve (BAV), a common congenital disorder, or in idiopathic cases such as patients with a normal tricuspid aortic valve (TAV). The main objective of our study was to identify shared and unique gene expression properties underlying the aortic dilation of BAV and TAV patients.
Unraveling divergent gene expression profiles in bicuspid and tricuspid aortic valve patients with thoracic aortic dilatation: the ASAP study.
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