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Deciphering isoform switching and specific isoform usage during biofilm lifestyle by Candida glabrata analysed through global transcriptomic approach

ABSTRACT: Deciphering isoform switching and specific isoform usage during biofilm lifestyle by Candida glabrata analysed through global transcriptomic approach

PROVIDER: PRJNA680327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13114664_1.fastq.gz	Fastqsanger.gz
	SRR13114664_2.fastq.gz	Fastqsanger.gz
	SRR13114665_1.fastq.gz	Fastqsanger.gz
	SRR13114665_2.fastq.gz	Fastqsanger.gz
	SRR13114666_1.fastq.gz	Fastqsanger.gz

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Deciphering isoform switching and specific isoform usage during biofilm lifestyle by Candida glabrata analysed through global transcriptomic approach

Project description:Methodology: RNA was extracted using Hi-PurA yeast RNA purification kit from biofilm and planktonic growth phase and sequenced by Illumina Hi-Seq 2500 and platform with 250bp paired chemistry and analysed by IsoformSwitchAnalyseR tool of bioconductor Results: Differential transcript expression (DTE) and differential transcript utilization (DTU) of C. glabrata showed that it utilized 292 significant transcripts isoforms during biofilm formation via isoform switching process. Conclusion: Investigation of the present study elucidated that the switched isoform and predicted proteins encoded in biofilm growth mode of this pathogen could be used as a potential target for the development of novel antifungal targets.

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

Project description:Transcriptome modulation is essential for metabolic adaptation to nutrient environments. However, the role of isoform usage, a crucial transcriptome component, is not yet fully understood. This study outlines the landscape of isoform usage modulations across major metabolic organs in both mice and monkeys, spanning diverse metabolic states. Our in-depth analysis identifies numerous isoform-usage events, intricately influenced by nutrient challenges and largely independent of gene expression regulation. Comparative analyses of mice and monkeys highlight hundreds of conserved isoform events that exhibit consistent responses to nutrient challenges across species and correlate with human metabolic traits. When analysing splicing factor-binding motifs in nutrient-regulated events, HuR emerges as the predominant orchestrator of the isoform network in adipocytes, which is validated using an adipose tissue-specific knockout and an Ap2-promoter-driven transgenic mouse model. In summary, our results offer a comprehensive perspective on isoform usage in metabolic regulation, setting a platform for future functional inquiries.

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Project description:This study outlines the landscape of isoform usage modulations across major metabolic organs in both mice and monkeys, spanning diverse metabolic states. Our in-depth analysis identify numerous isoform-usage events, intricately influenced by nutrient challenges and largely independent of gene expression regulation. When analysing splicing factor-binding motifs in nutrient-regulated events, HuR emerges as the predominant orchestrator of the isoform network in adipocytes.

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation (RIP-seq)

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Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

Project description:Isoform Usage as a Distinct Regulatory Layer Driving Nutrient-Responsive Metabolic Adaptation

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Genetic analysis of isoform usage in the human anti-viral response

Project description:While genetic variants are known to be associated with overall gene abundance in stimulated immune cells, less is known about their effects on alternative isoform usage. Analyzing RNA-seq profiles of monocyte-derived dendritic cells from 243 individuals, we uncovered thousands of unannotated isoforms synthesized in response to influenza infection and type 1 interferon stimulation. We identified more than a thousand quantitative trait loci (QTLs) associated with alternate isoform usage (isoQTLs), many of which are independent of expression QTLs for the same gene. Compared to eQTLs, isoQTLs are enriched for splice sites and untranslated regions, but depleted of sequences upstream of annotated transcription start sites. Both eQTLs and isoQTLs explain a significant proportion of the disease heritability attributed to common genetic variants.

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