Gladiolus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB15481 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR459504_1.fastq.gz | Fastqsanger.gz | |||
| DRR459504_2.fastq.gz | Fastqsanger.gz | |||
| DRR459505_1.fastq.gz | Fastqsanger.gz | |||
| DRR459505_2.fastq.gz | Fastqsanger.gz | |||
| DRR459506_1.fastq.gz | Fastqsanger.gz |
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Project description:Both exogenously supplied and transgenic induced cytokinin production can effectively delay senescence of broccoli florets during postharvest storage. However, a substantial comparison between the mechanisms of these two treatments on delaying broccoli florets senescence was absent. Here, we conduct microarray analysis on broccoli florets of N6-benzylaminopurine treated and ipt-transgenic broccoli that harbor a senescence-associated-gene promoter triggering isopentenyltransferase gene expression during postharvest storage.
2013-05-01 | GSE42609 | GEO
Project description:Both exogenously supplied and transgenic induced cytokinin production can effectively delay senescence of broccoli florets during postharvest storage. However, a substantial comparison between the mechanisms of these two treatments on delaying broccoli florets senescence was absent. Here, we conduct microarray analysis on broccoli florets of N6-benzylaminopurine treated and ipt-transgenic broccoli that harbor a senescence-associated-gene promoter triggering isopentenyltransferase gene expression during postharvest storage. Analysis used RNA of Green King inbred line 104 as control sample for comparison to the experimental samples of ipt-transgenic line 102, 103 and parental line Green King as well as 10 ppm BA treated Green King at harvest and after postharvest storage at 25 centigrade in the dark for 4 days.
2013-05-01 | E-GEOD-42609 | biostudies-arrayexpress
Project description:Coordinated functioning of the cob and florets of the maize ear confers grain yield. However, comprehensive molecular differentiation of the cob and florets and their responses to low nitrogen (LN) stress remain elusive. We compared transcriptional profiles of the cob and peripheral florets of a maize hybrid at the silking stage at two N levels in the field and found 1,864 differentially expressed genes between the cob and florets, with 1314 genes up-regulated in the cob and 550 genes up-regulated in florets. The cob was featured by preferential expression of 161 genes, with striking enrichment of genes that are involved in transport facilitation and energy metabolism, consistent with the physiological role of the cob in C/N storage and transfer during ear development. The florets were characteristic of preferential expression of 108 genes, with enrichment of genes that are involved in the cellular process and lipid biosynthetic process. LN caused differential expression of 588 genes in the cob and only 195 genes in florets, indicating that the cob dominated the response of the ear to LN at the transcriptional level. Differentially expressed genes under LN were involved in C/N metabolism, transcriptional regulation, development, cell rescue and defense, and signal transduction in the cob and/or florets. The expression level of 106 genes was regulated by LN in both tissues, suggesting a common regulatory network in these two functionally distinct tissues under LN. Compared with P or K deficiency, LN specifically caused differential expression of 14 genes, revealing unique biological consequences in the ear caused by N limitation at a critical reproductive stage. Collectively, our studies identified unique transcriptomic signatures of the cob and florets, revealed the dominance of the cob in response to LN at the silking stage, and provided molecular markers for N nutritional diagnosis and N efficient maize breeding.
2015-07-19 | GSE59613 | GEO
Project description:Although CD4 T cell senescence plays an important role in immunosenescence, the mechanisms remain unclear. We found that T cell-specific Menin deficiency results in the premature senescence of CD4 T cells, accompanied by the senescence-associated secretory phenotype (SASP) after antigenic stimulation. TH1 and TH2 differentiation was dysregulated in Menin-knockout CD4 T cells. Bach2, which regulates SASP and TH differentiation, was identified as a Menin target. Menin binds to the Bach2 locus, and controls its expression through maintenance of histone acetylation. These findings reveal a critical role of the Menin-Bach2 pathway in regulating CD4 T cell senescence and homeostasis, thus indicating the involvement of this pathway in the inhibition of age-associated development of inflammatory diseases, which are induced by immunosenescence. Examination of transcriptional factor Menin binding and histone modefications in Menin WT and KO CD4 T cells
2014-03-27 | E-GEOD-53831 | biostudies-arrayexpress
Project description:In the central spikelet, floret primordia proximal to rachis typically develop into fertile florets, while those distal ones tend to abort. However, the mechanisms driving these divergent outcomes remain unclear. To elucidate these differences, a two-year field experiment was conducted, analyzing the differences between fertile (floret 1) and abortive florets (floret 5) at phenotypic, physiological, cellular, and transcriptional levels. Our results showed that floret 1 (F1) developed earlier than floret 5 (F5), evidenced as distinct floret and anther cell morphology. This developmental difference was associated with distinct metabolic strategies: F1 prioritizes starch biosynthesis by enhancing photosynthetic efficiency and reducing thermal dissipation, while F5 diverts carbon to trehalose metabolism under resource constraints. Transcriptomic profiling revealed 17,711 differentially expressed genes, predominantly enriched in carbohydrate metabolism. Key starch-related genes (WAXY, SS, GBE1) were upregulated in F1, while trehalose synthesis genes (TPS, TPP) dominated in F5, reflecting a metabolic trade-off between growth and survival. Hormonal profiling revealed elevated indole-3-acetic acid (IAA) levels in F1, driven by upregulated genes encoding enzymes of TDC and YUCCA, whereas abscisic acid (ABA) level increased in F5, mediated by NCED. Specially, tissue-specific regulation in fertile floret was clarified: lemma tissues enriched in photosynthesis genes supplied localized carbon, anthers relied on sucrose cleavage genes to sustain pollen development, and ovaries activated lipid biosynthesis genes for embryogenesis. Collectively, we propose a model where IAA-starch synergy in proximal florets establishes a competitive metabolic sink, whereas ABA-T6P interplay in distal florets enforces developmental arrest, thereby optimizing resource allocation and reproductive success. The proposed regulatory framework provides novel views for improving floret fertility through carbohydrate partitioning and hormone signaling.
2025-06-03 | GSE291169 | GEO
Project description:This study investigates the role of Cathepsin D (CTSD) in diabetic vascular complications, particularly its impact on the phenotypic transformation of vascular smooth muscle cells (VSMCs) induced by advanced glycation end-products (AGEs), and explores its potential molecular mechanisms. CTSD was overexpressed in VSMCs using lentiviral vectors. Various methods, including CCK-8, immunofluorescence, SA-β-Gal staining, EdU assay, scratch assay, cell cycle analysis, and Western blotting, were employed to assess VSMC viability, proliferation, migration, senescence, and apoptosis. Additionally, transcriptomic and metabolomic analyses were conducted to investigate the molecular mechanisms underlying CTSD overexpression in VSMCs. AGEs treatment significantly inhibited CTSD expression in VSMCs, leading to reduced cell viability, enhanced proliferation and migration, increased senescence, and apoptosis. In contrast, overexpression of CTSD effectively inhibited AGEs-induced VSMC proliferation, migration, senescence, and apoptosis. Combined transcriptomic and metabolomic analyses suggested that CTSD may affect VSMC phenotypic transformation by inhibiting the glycolysis pathway. This study highlights the critical role of CTSD in the phenotypic transformation of VSMCs induced by AGEs and provides a new perspective for cardiovascular and cerebrovascular disease treatment. CTSD may emerge as a novel therapeutic target, though its specific molecular mechanisms and clinical application prospects in VSMC phenotypic transformation require further investigation.
2025-04-09 | GSE278266 | GEO
Project description:Aging associates with progressive loss of skeletal muscle function leading up to sarcopenia, a process characterized by impaired mobility and weakening of muscle strength. Molecular mechanisms underpinning sarcopenia are still poorly characterized. Since aging associates with profound epigenetic changes, epigenetic landscape alteration analysis in the skeletal muscle promises to highlight molecular mechanisms of age-associated sarcopenia. The study was conducted exploiting the short-lived Nothobranchius furzeri (Nfu), a relatively new model for aging studies. The epigenetic analysis suggested for a less accessible and more condensed chromatin structure in old Nfu skeletal muscle. Specifically, an accumulation of heterochromatin regions was observed as consequence of increased levels of H3K27me3, HP1a, polycomb complex subunits and senescence associated heterochromatic foci (SAHFs). Consistently, euchromatin histone marks, including H3K9ac, decreased. The integrative bioinformatics analysis of RNASeq and ChIPSeq, related to skeletal muscle of Nfu at different ages, revealed a down-modulation of transcripts involved in cell cycle, differentiation and DNA repair and an up-regulation of inflammation and senescence genes. Undoubtedly, more studies are needed to disclose the detailed mechanisms, but this approach shed light on unprecedented specific features of Nfu skeletal muscle aging, potentially associated with sarcopenia onset and consequent impairment of swimming and mobility typical of old Nfu.
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Project description:Identification of heterogeneous senescence-associated transcriptional programs
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Project description:Cellular senescence is a complex biological process that contributes to wound healing, carcinogenesis, and age-related disease. Although the molecular mechanisms whereby senescence promotes wound repair are not well understood, the protein ANKRD1, which promoted wound healing in mice, was found to increase in senescent cells. We hypothesized that ANKRD1 may play a role in senescence-mediated wound healing. Conditioned medium (CM) from senescent WI-38 human diploid fibroblasts hastened cell migration of human HaCaT keratinocytes. Interestingly, silencing ANKRD1 in WI-38 cells reduced the effect of CM on cell migration, while overexpressing ANKRD1 accelerated it. Further proteomic analysis revealed that ANKRD1 associates with YBOX1, a multifunctional protein that modulates transcription of the ELN gene and reduces ELN mRNA production. The product of the ELN gene, the protein ELN or tropoelastin (a subunit of elastin), is a secreted factor that reduces motility. Thus, we propose that a rise in ANKRD1 during early senescence transiently limits the YBOX1-dependent transcriptional increase in ELN production, and thereby enables cell motility in early phases of senescence.
2023-06-01 | MSV000092079 | MassIVE
Project description:Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are interdependent has not been thoroughly studied. We hypothesize that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. In this study, we show that BMAL1 in is uniquely localized to genomic motifs associated with AP-1 in senescent cells and contributes to AP-1 transcriptional control of the senescence program.
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