Gene expression and H3K27 tri-methylation analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE24507 | GEO | 2011/04/20
SECONDARY ACCESSION(S): PRJNA132493
REPOSITORIES: GEO
Similar Datasets
Project description:For the histone methylation analysis of undifferentiated and differentiated tissues a meristem enriched fraction and young leaves (up to 3 mm leaf blade length) were isolated from clavata3-9 plants. Clavata3-9 mutants harbour larger shoot apical meristems than wild type plants enabling the preparation of meristematic tissue by manual dissection. Samples from both tissues were used for expression and histone H3 lysine 27 trimethylation (H3K27me3) analysis. Tissues for expression and H3K27me3 ChIP-chip analyses were simultaneously harvested.
2011-03-21 | GSE24474 | GEO
Project description:For the histone methylation analysis of undifferentiated and differentiated tissues a meristem enriched fraction and young leaves (up to 3 mm leaf blade length) were isolated from clavata3-9 plants. Clavata3-9 mutants harbour larger shoot apical meristems than wild type plants enabling the preparation of meristematic tissue by manual dissection. Samples from both tissues were used for expression and histone H3 lysine 27 trimethylation (H3K27me3) analysis. Tissues for expression and H3K27me3 ChIP-chip analyses were simultaneously harvested. Meristem enriched samples (Me1 and Me2) and young leaf samples (Le1 and Le2) of clavata3-9 plants were isolated and hybridised to whole genome tiling arrays [platform GPL3371]. Two biological replicates were performed.
2011-03-21 | E-GEOD-24474 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE24464: Expression analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants GSE24474: H3K27 tri-methylation analysis of meristematic tissue (Me) and young leaves (Le) isolated by manual dissection of clv3-9 plants Refer to individual Series
2011-04-20 | E-GEOD-24507 | biostudies-arrayexpress
Project description:For the expression analysis of undifferentiated and differentiated tissues a meristem enriched fraction and young leaves (up to 3 mm leaf blade length) were isolated from clavata3-9 plants. Clavata3-9 mutants harbour larger shoot apical meristems than wild type plants enabling the preparation of meristematic tissue by manual dissection. Samples from both tissues were used for expression and histone H3 lysine 27 trimethylation (H3K27me3) analysis. Tissues for expression and H3K27me3 ChIP-chip analyses were simultaneously harvested.
2011-03-21 | GSE24464 | GEO
Project description:For the expression analysis of undifferentiated and differentiated tissues a meristem enriched fraction and young leaves (up to 3 mm leaf blade length) were isolated from clavata3-9 plants. Clavata3-9 mutants harbour larger shoot apical meristems than wild type plants enabling the preparation of meristematic tissue by manual dissection. Samples from both tissues were used for expression and histone H3 lysine 27 trimethylation (H3K27me3) analysis. Tissues for expression and H3K27me3 ChIP-chip analyses were simultaneously harvested. Meristem enriched samples (XMe1 and XMe2) and young leaf samples (XLe1 and XLe2) of clavata3-9 plants were isolated and hybridised to Agilent 44 k arrays [G2519F, V4 (Agilent, Santa Clara)]. Two biological replicates were performed.
2011-03-21 | E-GEOD-24464 | biostudies-arrayexpress
Project description:Sugar allocation from source to sink (young) leaves, critical for plant development, relies on activities of plasma membrane sugar transporters. However, the key sugar unloading mechanism to sink leaves remains elusive. SWEET transporters mediate sugar efflux into reproductive sinks; therefore, they are promising candidates for sugar unloading during leaf growth. Transcripts of SlSWEET1a, belonging to clade I of the SWEET family, were markedly more abundant than those of all other 30 SlSWEET genes in young leaves of tomatoes. High expression of SlSWEET1a was also detected in reproductive sinks, such as flowers. SlSWEET1a was dominantly expressed in leaf unloading veins, and the green fluorescent protein (GFP) fusion protein was localized to the plasma membrane using Arabidopsis protoplasts, further implicating this carrier in sugar unloading. In addition, yeast growth assays and radiotracer uptake analyses further demonstrated that SlSWEET1a acted as a low-affinity (Km ~100 mM) glucose-specific carrier with a passive diffusion manner. Finally, virus-induced gene silencing of SlSWEET1a expression reduced hexose accumulation to ~50% in young leaves, with a parallel 2-fold increase in mature leaves. Thus, we propose a novel function for SlSWEET1a in the uptake of glucose into unloading cells as part of the sugar unloading mechanism in sink leaves of tomato.
| S-EPMC6598072 | biostudies-literature
Project description:The adaptation of the lungs to air breathing at birth requires the fine orchestration of different processes to control lung morphogenesis and progenitor cell differentiation. However, there is little understanding of the role that epigenetic modifiers play in the control of lung development. We found that the histone methyl transferase Ezh2 plays a critical role in lung lineage specification and survival at birth. We performed a genome-wide transcriptome study combined with a genome-wide analysis of the distribution of H3K27 tri-methylation marks to interrogate the role of Ezh2 in lung epithelial cells. Lung cells isolated from Ezh2-deficient and control mice at embryonic day E16.5 were sorted into epithelial and mesenchymal populations based on EpCAM expression. This enabled us to dissect the transcriptional and epigenetic changes induced by the loss of Ezh2 specifically in the lung epithelium. Here we provide a detailed description of the analysis of the RNA-seq and ChIP-seq data, including quality control, read mapping, differential expression and differential binding analyses, as well as visualisation methods used to present the data. These data can be accessed from the Gene Expression Omnibus database (super-series accession number GSE57393).
| S-EPMC4583701 | biostudies-literature
Project description:This study compares the epigenetic signatures of CD34+ cells from chronic phase chronic myeloid leukemia (CML) samples and blast phase CML samples v.s. normal CD34+ cells from cord blood and adult bone marrow samples. H3K27me3 genomic loci were detected by ChIP-seq.
2021-11-08 | GSE188241 | GEO
Project description:BackgroundAlkali stress is an important agricultural contaminant and has complex effects on plant metabolism. The aim of this study was to investigate whether the alkali stress has different effects on the growth, ion balance, and nitrogen metabolism in old and young leaves of rice plants, and to compare functions of both organs in alkali tolerance.Methodology/principal findingsThe results showed that alkali stress only produced a small effect on the growth of young leaves, whereas strongly damaged old leaves. Rice protected young leaves from ion harm via the large accumulation of Na(+) and Cl(-) in old leaves. The up-regulation of OsHKT1;1, OsAKT1, OsHAK1, OsHAK7, OsHAK10 and OsHAK16 may contribute to the larger accumulation of Na(+) in old leaves under alkali stress. Alkali stress mightily reduced the NO(3)(-) contents in both organs. As old leaf cells have larger vacuole, under alkali stress these scarce NO(3)(-) was principally stored in old leaves. Accordingly, the expression of OsNRT1;1 and OsNRT1;2 in old leaves was up-regulated by alkali stress, revealing that the two genes might contribute to the accumulation of NO(3)(-) in old leaves. NO(3)(-) deficiency in young leaves under alkali stress might induce the reduction in OsNR1 expression and the subsequent lacking of NH(4)(+), which might be main reason for the larger down-regulation of OsFd-GOGAT and OsGS2 in young leaves.Conclusions/significanceOur results strongly indicated that, during adaptation of rice to alkali stress, young and old leaves have distinct mechanisms of ion balance and nitrogen metabolism regulation. We propose that the comparative studies of young and old tissues may be important for abiotic stress tolerance research.
| S-EPMC3360002 | biostudies-literature
Project description:Acute lung injury (ALI) is a common critical disease, which is characterized by an uncontrolled, acute inflammatory response, diffuse lung damage and ultimately directly deteriorates into acute respiratory distress syndrome. The number of pro-inflammatory macrophages is related to the severity of ALI. Up-regulation of lipopolysaccharide (LPS)-activated macrophage apoptosis can reduce the pro-inflammatory reactions. Jumonji domain-containing protein D3 (JMJD3)-mediated histone 3 lysine 27 trimethylation (H3K27me3) demethylation may promote the pro-inflammatory response of macrophages under LPS stimulation. However, the mechanism of JMJD3 affecting macrophage apoptosis is still not clear. To explore this gap in knowledge, the ALI mice model with intratracheal administration of LPS and RAW264.7 cells with LPS stimulation were used as in vivo and in vitro experiments. The expression of JMJD3 and H3K27me3 and their cellular localization were analysed in lung tissue. Apoptosis was evaluated using TUNEL staining and flow cytometry. Expression of H3K27me3, ADORA2A and C/EBPβ were compared among different treatments and chromatin immunoprecipitation was performed to investigate the regulatory relationship. Our study showed that JMJD3 expression was upregulated in LPS-induced ALI mice and RAW264.7 cells. JMJD3-indued H3K27me3 demethylation inhibited caspase-3 cleavage by upregulating ADORA2A to decrease LPS-stimulated macrophage apoptosis and promoted the inflammatory reaction. This H3K27me3 demethylation also increased C/EBPβ expression, which may enhance ADORA2A expression further. Besides, inhibiting ADORA2A can also promote LPS-limited macrophage apoptosis. Moreover, the inhibition of JMJD3 in vivo and in vitro relieved the inhibition of macrophage apoptosis thus leading to the resolution of the inflammation. JMJD3 might inhibit macrophage apoptosis by promoting ADORA2A expression in LPS-induced ALI.
| S-EPMC9715944 | biostudies-literature