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Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention

ABSTRACT: Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention

PROVIDER: PRJNA1060673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27408514_1.fastq.gz	Fastqsanger.gz
	SRR27408514_2.fastq.gz	Fastqsanger.gz
	SRR27408515_1.fastq.gz	Fastqsanger.gz
	SRR27408515_2.fastq.gz	Fastqsanger.gz
	SRR27408516_1.fastq.gz	Fastqsanger.gz

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Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention

Project description:Type 2 Diabetes (T2D) is a global health issue characterized by abnormal blood glucose levels and often associated with excessive hepatic gluconeogenesis. Increased circulating non-essential amino acids (NEAAs) are consistently observed in T2D individuals; however, the specific contribution of each amino acid to T2D pathogenesis remains less understood. Here, we reported an unexpected role of the NEAA proline in coordinating hepatic glucose metabolism by modulating paraspeckle, a nuclear structure scaffolded by the long noncoding RNA Neat1. Mechanistically, proline diminished paraspeckles in hepatocytes, liberating the retained mRNA species into cytoplasm for translation, including the mRNAs of Ppargc1a and Foxo1, contributing to enhanced gluconeogenesis and hyperglycemia. We further demonstrated that the proline-paraspeckle-mRNA retention axis existed in diabetic liver samples, and intervening this axis via paraspeckle restoration significantly alleviated hyperglycemia in both female and male diabetic mouse models. Collectively, our results not only delineated a previously unappreciated proline-instigated, paraspeckle-dependent mRNA retention mechanism regulating gluconeogenesis, but also spotlighted proline and paraspeckle as potential targets for managing hyperglycemia. This SuperSeries is composed of the SubSeries listed below.

2024-11-26 | GSE252452 | GEO

Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [lncRNA-Seq]

2024-11-26 | GSE252451 | GEO

Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [RIP-Seq]

2024-11-26 | GSE252450 | GEO

Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [RIP-Seq]

Project description:Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [RIP-Seq]

| PRJNA1060669 | ENA

Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [lncRNA-Seq]

Project description:Proline exacerbates hepatic gluconeogenesis via paraspeckle-dependent mRNA retention [lncRNA-Seq]

| PRJNA1060680 | ENA

Direct RNA-RNA interaction between Neat1 and RNA targets, as a mechanism for RNAs paraspeckle retention

Project description:Direct RNA-RNA interaction between Neat1 and RNA targets, as a mechanism for RNAs paraspeckle retention

| PRJNA671727 | ENA

Direct RNA-RNA interaction between Neat1 and RNA targets, as a mechanism for RNAs paraspeckle retention

Project description:The goal of this study was to determine if the lncRNA Neat1, in addition to its structural role, may also be directly involved in the binding by base pairing of RNAs and consequently in their retention in paraspeckles

2021-04-21 | GSE160069 | GEO

Paraspeckle-Independent Co-Transcriptional Regulation of Nuclear microRNA Biogenesis by SFPQ [PRO-seq]

Project description:MicroRNAs (miRNAs) play crucial roles in physiological functions and diseases such as cancer, but the regulation of their nuclear biogenesis remains poorly understood. Here, BioID on Drosha, the catalytic subunit of the microprocessor complex, revealed its proximity to SFPQ, a multifunctional RNA-binding protein (RBP) notably involved in forming the paraspeckle nuclear condensates. SFPQ depletion impacted both primary and mature miRNA expression, while other crucial paraspeckle proteins or the paraspeckle scaffolding lncRNA NEAT1 did not, indicating a unique paraspeckle-independent role. Comprehensive transcriptomic analyses showed that SFPQ loss broadly affects RNA and miRNA host gene (miRNA HG) expression, influencing both their transcription and stability. Notably, SFPQ protects specific miRNA HGs, including the oncogenic miR-17~92 polycistron, from degradation by the nuclear NEXT-exosome complex. Lastly, we show that high SFPQ is tightly linked with overexpression miR-17~92 and its mature miRNAs across a broad variety of cancers. Our findings reveal a dual role for SFPQ in the regulation of miRNA HGs transcription and stability, as well as its significance in cancers.

2024-09-04 | GSE262127 | GEO