Arum concinnatum
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR023772_1.fastq.gz | Fastqsanger.gz | |||
| DRR023772_2.fastq.gz | Fastqsanger.gz | |||
| DRR023773_1.fastq.gz | Fastqsanger.gz | |||
| DRR023773_2.fastq.gz | Fastqsanger.gz | |||
| DRR023774_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Senescence is genetically-controlled and activated in mature tissues during ageing. However, immature plant tissues also display senescence-like symptoms when continuously exposed to adverse energy-depleting conditions. We used detached dark-held immature inflorescences of Arabidopsis thaliana to understand the metabolic reprogramming occurring in immature tissues transitioning from rapid growth to precocious senescence. Macroscopic growth of the detached inflorescences rapidly ceased upon placement in water in the dark at 21°C. Inflorescences were completely de-greened by 120 h of dark incubation and by 24 h had already lost 24% of their chlorophyll and 34% of their protein content. Comparative transcriptome profiling at 24 h revealed that inflorescences response at 24 h had a large carbon-deprivation component. Genes that positively regulate developmental senescence (ANAC092) and shade avoidance syndrome (PIF4 and PIF5) were up-regulated within 24 h. Mutations in these genes delayed de-greening of the inflorescences. Their up-regulation was suppressed in dark-held inflorescences by glucose treatment, which promoted macroscopic growth and development and inhibited de-greening of the inflorescences. Detached inflorescences held in the dark for 4 days were still able to re-initiat development to produce siliques upon being brought out to light indicating the transcriptional reprogramming at 24 h was adaptive and reversible. Our results suggest that the response of detached immature tissues to dark storage involves interactions between carbohydrate status sensing and light deprivation signaling and that the dark adaptive response of the tissues appears to utilize some of the same key regulators as developmental senescence.
2012-09-25 | GSE41099 | GEO
Project description:The common fig cultivar Zibao, planted at the Shangzhuang Experimental Station of China Agricultural University (Peking, China). Based on the three fig development phases (Flaishman et al., 2008), we subdivided the fig development process into six stages: stages 1 and 2 belonging to phase Ⅰ, a rapid growth stage; stages 3 and 4 belonging to phase Ⅱ, during which fruit size and hardness remain almost unchanged; stages 5 and 6 belonging to phase Ⅲ, the mature stage, where stage 5 corresponded to commercial ripeness. Inflorescences and receptacles at each stage were separated, marked as F1–F6 and R1–R6, respectively. Stage 1, 3 and 5 inflorescences and receptacles were used for proteomic analysis.
2021-05-01 | PXD025170 | Pride
Project description:Comparion of gene expression profiles of wild-type and apetala1 inflorescences The gene expression profile of inflorescences of the floral homeotic mutant apetala1 was compared to wild-type inflorescences (Ler) using a whole-genome oligonucleotide array (Agilent, custom-commercial). Experiment was performed in triplicate.
2010-04-02 | GSE20138 | GEO
Project description:Senescence is genetically-controlled and activated in mature tissues during ageing. However, immature plant tissues also display senescence-like symptoms when continuously exposed to adverse energy-depleting conditions. We used detached dark-held immature inflorescences of Arabidopsis thaliana to understand the metabolic reprogramming occurring in immature tissues transitioning from rapid growth to precocious senescence. Macroscopic growth of the detached inflorescences rapidly ceased upon placement in water in the dark at 21M-BM-0C. Inflorescences were completely de-greened by 120 h of dark incubation and by 24 h had already lost 24% of their chlorophyll and 34% of their protein content. Comparative transcriptome profiling at 24 h revealed that inflorescences response at 24 h had a large carbon-deprivation component. Genes that positively regulate developmental senescence (ANAC092) and shade avoidance syndrome (PIF4 and PIF5) were up-regulated within 24 h. Mutations in these genes delayed de-greening of the inflorescences. Their up-regulation was suppressed in dark-held inflorescences by glucose treatment, which promoted macroscopic growth and development and inhibited de-greening of the inflorescences. Detached inflorescences held in the dark for 4 days were still able to re-initiat development to produce siliques upon being brought out to light indicating the transcriptional reprogramming at 24 h was adaptive and reversible. Our results suggest that the response of detached immature tissues to dark storage involves interactions between carbohydrate status sensing and light deprivation signaling and that the dark adaptive response of the tissues appears to utilize some of the same key regulators as developmental senescence. Detached arabidopsis inflorescences were harvested and either immediately snap-frozen in liquid nitrogen and stored at -80M-BM-0C, or placed at 21M-BM-0C on blotting paper moistened with water inside a 2-L black plastic container for RNA extraction and hybridization on Affymetrix microarrays. Ten inflorescences from 10 independent plants were pooled for each time point (0 h or 24 h).
2012-09-25 | E-GEOD-41099 | biostudies-arrayexpress
Project description:Early B Cell Factor 2 (EBF2) is required for brown adipose tissue basal thermogenic gene expression; however, it was unknown whether chronic cold exposure normalized the expression of thermogenic genes in Ebf2 mutant mice. We examined the transcriptome of Ebf2 WT and mutant brown adipose tissue in mice housed at room temperature or one week of cold exposure.
2020-03-23 | GSE144186 | GEO
Project description:Medium conditioned by LLC cells stimulates thermogenic gene expression when added onto primary adipocytes. We generated single cell colonies from parental LLC cells. Media conditioned by the subclones stimulated thermogenic gene expression in primary adipocytes at varying degrees. Subclones 2, 3, 6 and 28 produce significantly larger amount of thermogenic activity than the subclones 18, 19, 23 and 24. We compared gene expression profiles of these subclones to identify secreted factors enriched in the more thermogenic clones. LLC subclones were cultured under conditioned medium preparation conditiones and total RNA was extracted from biological replicates.
2014-07-13 | E-GEOD-57797 | biostudies-arrayexpress
Project description:Mitochondrial proteases are emerging as key regulators of mitochondrial plasticity acting both as protein quality surveillance and regulatory enzymes by performing highly regulated proteolytic reactions. It remains unclear, however, whether the regulated mitochondrial proteolysis is mechanistically linked to cell identity switch such as white-to-beige conversion of adipocytes. We found that disruption of LONP1-dependent proteolysis substantially impairs thermogenic molecular program and cellular respiration in in vitro differentiated primary adipocytes. qPCR analysis showed that expression levels of Ucp1 and other beige adipocyte thermogenic genes were remarkably downregulated in LONP1 AKO adipocytes. We took a deeper dive into the characterization of histone modifications in LONP1 AKO adipocytes using the global enhancer marker H3K4me1 ChIP-Seq. These unbiased ChIP seq data are strong evidence of that LONP1 loss results in decreased H3K4me1 on a broad array of thermogenic genes. These results collectively indicate that LONP1 is crucial to maintain proper epigenetic homeostasis and beige thermogenic gene expression.
2023-04-08 | GSE222490 | GEO
Project description:Energy-storing white adipocytes maintain their identity by suppressing the gene program defining energy-burning thermogenic brown/beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional co-regulator ZFP423 and brown/beige cell determination factor, EBF2, is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread “browning” of WAT in adult mice. Mechanistically, adipocyte Zfp423 deficiency induces an EBF2 NuRD-to-BAF co-regulator switch and a shift in PPARgamma occupancy to thermogenic genes. This shift in PPARgamma occupancy increases the anti-diabetic efficacy of the PPARgamma agonist rosiglitazone in obesity while diminishing the unwanted weight-gaining effect of the drug. These data indicate that ZFP423 controls EBF2 co-activator recruitment and PPARgamma occupancy to determine the thermogenic plasticity of adipocytes and raise the concept of targeting transcriptional brakes in adipocyte gene expression as a therapeutic strategy to induce thermogenic adipocyte biogenesis in obesity.
2022-05-01 | GSE175654 | GEO
Project description:Energy-storing white adipocytes maintain their identity by suppressing the gene program defining energy-burning thermogenic brown/beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional co-regulator ZFP423 and brown/beige cell determination factor, EBF2, is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread “browning” of WAT in adult mice. Mechanistically, adipocyte Zfp423 deficiency induces an EBF2 NuRD-to-BAF co-regulator switch and a shift in PPARgamma occupancy to thermogenic genes. This shift in PPARgamma occupancy increases the anti-diabetic efficacy of the PPARgamma agonist rosiglitazone in obesity while diminishing the unwanted weight-gaining effect of the drug. These data indicate that ZFP423 controls EBF2 co-activator recruitment and PPARgamma occupancy to determine the thermogenic plasticity of adipocytes and raise the concept of targeting transcriptional brakes in adipocyte gene expression as a therapeutic strategy to induce thermogenic adipocyte biogenesis in obesity.
2022-05-01 | GSE175653 | GEO