Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1089524 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28385886.fastq.gz | Fastqsanger.gz | |||
| SRR28385887.fastq.gz | Fastqsanger.gz | |||
| SRR28385888.fastq.gz | Fastqsanger.gz | |||
| SRR28385889.fastq.gz | Fastqsanger.gz | |||
| SRR28385890.fastq.gz | Fastqsanger.gz |
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Project description:Rhododendron is well known woody plant, as having high ornamental and economic values. Heat stress is one of the important environmental stresses that effects Rhododendron growth. Recently, melatonin was reported to alleviate abiotic stress in plants. However, the role of melatonin in Rhododendron is still unknown. In the present study, the effect of melatonin on Rhododendron under heat stress and the potential mechanism was investigated. Through morphological characterization and chlorophyll a fluorescence analysis, 200µM was selected for the best melatonin concentration to mitigate heat stress in Rhododendron. To reveal the mechanism of melatonin priming alleviating the heat stress, the photosynthesis indexes, Rubisco activity and ATP content were detected in 25 ℃, 35 ℃ and 40 ℃. The results showed that melatonin improves electron transport rate (ETR), PSII and PSI activity, Rubisco activity and ATP content under high temperature stress. Furthermore, transcriptome analysis showed that a significant enrichment of differentially expressed genes in the photosynthesis pathway, and most of genes in photosynthesis pathway displayed a more significantly slight down-regulation under high temperature stress in melatonin-treatment plants, compared with melatonin-free plants. We identified PGR5……Together, these results demonstrate that melatonin could promote the photosynthetic electron transport, improve the enzymes activities in Calvin cycle and the production of ATP, and thereby increase photosynthetic efficiency and CO2 assimilation capacity under heat stress, through regulating the expression of some key genes, such as PGR5…Therefore, melatonin application displayed great potential to cope with the heat stress in Rhododendron.
2024-09-30 | GSE214428 | GEO
Project description:Lack of resistance to pink snow mould (Microdochium nivale) is seen as a major constraint for adaptation of perennial ryegrass (Lolium perenne L.) at higher latitudes. Plants generally become more resistant to snow moulds after cold acclimation, and almost all investigations of genetic variation in resistance have been performed using cold acclimated plants. However, there may be variation in resistance mechanisms that are functioning independently of cold acclimation. In this study our aim was to identify candidate genes involved in such resistance mechanisms. We first characterized variation in resistance to M. nivale among non-acclimated plants of eight genotypes from the Norwegian cultivar Fagerlin and selected one resistant and one susceptible genotype for transcriptome analysis. Total RNA was extracted from leaf blade tissue of plants exposed to three different treatments: non-inoculated and non-incubated plants, non-inoculated plants after four days of incubation, and inoculated plants after four days of incubation. cDNA libraries were prepared and paired-end sequencing performed using Illumina Hiseq 2000. Transcriptome profiles, GO enrichment and KEGG pathway analysis indicate that defence response related genes are differentially expressed between incubated non-inoculated and incubated inoculated conditions both within resistant and susceptible genotypes. A significant up-regulation of defence related genes as well as genes involved in cell wall cellulose metabolic processes and aryl-alcohol dehydrogenase (NADP+) activity was observed in the resistant genotype. The candidate genes identified in this study might be potential molecular marker resources for breeding perennial ryegrass cultivars with improved resistance to pink snow mould.
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Project description:Epidemiological investigations have revealed a significant association between alcohol consumption and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Nevertheless, the potential mechanisms are still inadequately revealed. This research aimed to investigate the impact of alcohol on CP/CPPS using an animal model and to elucidate the underlying mechanisms. We first established the widely used animal model for CP/CPPS, experimental autoimmune prostatitis (EAP). During the induction of EAP, mice were fed with alcohol or control diet. The HE staining, ELISA, and behavioral experiments were employed to assess the severity of inflammation in EAP mice and EAP-alcohol mice. Patients with a history of chronic alcohol consumption were also included to evaluate the effects of chronic alcohol consumption on CP/CPPS. Subsequently, proteomic analysis, flow cytometry, immunofluorescence, Western blotting, and immunohistochemistry were utilized to investigate the underlying mechanism involved both in vivo and in vitro. HE staining, ELISA, and behavioral experiments showed that alcohol exacerbated the severity of EAP in mice and patients. Proteomic and KEGG pathway analyses showed that abnormal Th1 differentiation and PI3K/AKT/mTOR pathway were significantly enriched. Subsequent mechanistic research showed that alcohol significantly activated PI3K/AKT/mTOR pathway andincreased the Th1 cell differentiation both in vivo and in vitro. In contrast, PI3K inhibitor LY294002 and shRNA-PI3K plasmid inhibited PI3K/AKT/mTOR pathway activation, reduced Th1 cell differentiation, and alleviated EAP inflammation severity, respectively. Our study is the first to demonstrate that alcohol intake promotes Th1 cell differentiation and exacerbates EAP by activating the PI3K/AKT/mTOR pathway. Additionally, the role of LY294002 in inhibiting PI3K/AKT/mTOR pathway to relieve EAP suggests that it can serveas a promising therapeutic target for CP/CPPS.
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Project description:Apicomplexan parasites use Ca2+-regulated exocytosis to secrete essential virulence factors from specialized organelles called micronemes. Ca2+-dependent protein kinases (CDPKs) are required for microneme exocytosis; however, the molecular events that regulate trafficking and fusion of micronemes with the plasma membrane remain unresolved. Here, we combine sub-minute resolution phosphoproteomics and bio-orthogonal labeling of kinase substrates in Toxoplasma gondii to identify 163 proteins phosphorylated in a CDPK1-dependent manner. In addition to known regulators of secretion, we identify uncharacterized targets with predicted functions across signaling, gene expression, trafficking, metabolism, and ion homeostasis. One of the CDPK1 targets is a putative HOOK activating adaptor. In other eukaryotes, HOOK homologs form the FHF complex with FTS and FHIP to activate dynein-mediated trafficking of endosomes along microtubules. We show the FHF complex is partially conserved in T. gondii, consisting of HOOK, an FTS homolog, and two parasite-specific proteins (TGGT1_306920 and TGGT1_316650). CDPK1 kinase activity and HOOK are required for the rapid apical trafficking of micronemes as parasites initiate motility. Moreover, parasites lacking HOOK or FTS display impaired microneme protein secretion, leading to a block in the invasion of host cells. Taken together, our work provides a comprehensive catalog of CDPK1 targets and reveals how vesicular trafficking has been tuned to support a parasitic lifestyle.
2023-10-18 | PXD039432 | Pride
Project description:Apicomplexan parasites use Ca2+-regulated exocytosis to secrete essential virulence factors from specialized organelles called micronemes. Ca2+-dependent protein kinases (CDPKs) are required for microneme exocytosis; however, the molecular events that regulate trafficking and fusion of micronemes with the plasma membrane remain unresolved. Here, we combine sub-minute resolution phosphoproteomics and bio-orthogonal labeling of kinase substrates in Toxoplasma gondii to identify 163 proteins phosphorylated in a CDPK1-dependent manner. In addition to known regulators of secretion, we identify uncharacterized targets with predicted functions across signaling, gene expression, trafficking, metabolism, and ion homeostasis. One of the CDPK1 targets is a putative HOOK activating adaptor. In other eukaryotes, HOOK homologs form the FHF complex with FTS and FHIP to activate dynein-mediated trafficking of endosomes along microtubules. We show the FHF complex is partially conserved in T. gondii, consisting of HOOK, an FTS homolog, and two parasite-specific proteins (TGGT1_306920 and TGGT1_316650). CDPK1 kinase activity and HOOK are required for the rapid apical trafficking of micronemes as parasites initiate motility. Moreover, parasites lacking HOOK or FTS display impaired microneme protein secretion, leading to a block in the invasion of host cells. Taken together, our work provides a comprehensive catalog of CDPK1 targets and reveals how vesicular trafficking has been tuned to support a parasitic lifestyle.
2023-10-18 | PXD039426 | Pride