Ontology highlight
ABSTRACT:
PROVIDER: PRJNA995182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25296833_1.fastq.gz | Fastqsanger.gz | |||
| SRR25296833_2.fastq.gz | Fastqsanger.gz | |||
| SRR25296834_1.fastq.gz | Fastqsanger.gz | |||
| SRR25296834_2.fastq.gz | Fastqsanger.gz | |||
| SRR25296835_1.fastq.gz | Fastqsanger.gz |
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Project description:Dwarfed stature is a desired trait for modern orchard production systems. One effective strategy of dwarfing is exogenously applying plant growth retardants (PGRs) to plants. However, for many economic fruit trees, the current knowledge on the regulatory mechanisms underlying the dwarfing effect of PGRs were limited, which largely restricts their agricultural application. In this study, we exogenously applied three kinds of PGRs (paclobutrazol, B9 and mannitol) to the seedlings of pomegranate (Punica granatum L.) and performed comparative transcriptome analysis to elucidate the molecular features of PGR-induced dwarfing in pomegranates. Our results showed that all the three PGRs could significantly suppress auxin biosynthetic and metabolic processes, as well as auxin-mediated shoot development, which may be the main reason for the dwarfing. Besides, different PGRs were also found to induce dwarfing via specially mechanisms. Cellular response to strigolactone were downregulated by the application of paclobutrazol, while carbohydrate homeostasis and metabolism were specifically suppressed in conditions of either B9 or mannitol treatments. Furthermore, exogenous PGR application was supposed to causes adverse impacts on the normal physiological process of pomegranate seedlings, which may bring extra burden to stress adaptation of pomegranate plants. These novel findings unveiled the genetic basis underlying the dwarfing in pomegranates.
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Project description:A spontaneously phenotypically degenerated strain of M. robertsii strain ARSEF 2575 (M. robertsii lc2575; lc = low conidiation) showed a reduction in conidiation and fungal virulence after successive subculturing on artificial medium. However, the conidial production and fungal virulence of a phenotypically degenerated M. robertsii were recovered by serially passaging through a plant host. The DNA methylation level of phenotypically degenerated Metarhizium robertsii M. robertsii lc2575 and this fungi after solider bean passages were tested through the whole genome bisulfite sequencing. The results showed that approximately 0.379 % of cytosines are methylated in the fungi after bean passages, almost the same as the DNA methylation level in M. robertsii lc2575 (0.375%). The distribution of different methylated regions located more on intergenic regions of fungi after bean passages than M. robertsii lc2575. Gene Ontology (GO) analysis and KEGG analysis of DMR-associated genes revealed that amino acid, carbohydrate and fatty acid metabolism.
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Project description:Pomegranate exhibits pronounced hypolipidemic properties, and the objective of this study was to delineate the precise mechanism by which pomegranate facilitates the treatment of hyperlipidemia.SD rats were fed with a high fat diet (HFD) to establish an hyperlipidemia model and intervened with pomegranate .Pomegranate significantly lowered body weight gain , liver weight and adipose tissue coefficient, and attenuated the hepatic steatosis.Serum concentrations of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were markedly reduced, concomitant with a significant elevation in high-density lipoprotein cholesterol (HDL-C) levels. Metabolomic analysis revealed that pomegranate treatment significantly modulated 37 metabolites linked to hyperlipidemia, with the primary pathways affected encompassing sphingolipid metabolism, pyrimidine metabolism, and arachidonic acid metabolism. Transcriptomic profiling identified 439 genes differentially expressed following pomegranate treatment, which were associated with various lipid-related and inflammatory pathways, predominantly including the lipid and atherosclerosis signaling pathway, NF-κB signaling pathway, and TNF signaling pathway.
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