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RNA-seq analysis of dark-induced senescence of the leaves of Ran-GDP and Ran-GTP overexpression transgenic plants

ABSTRACT: RNA-seq analysis of dark-induced senescence of the leaves of Ran-GDP and Ran-GTP overexpression transgenic plants

PROVIDER: PRJNA725265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14328019.fastq.gz	Fastqsanger.gz
	SRR14328020.fastq.gz	Fastqsanger.gz
	SRR14328021.fastq.gz	Fastqsanger.gz
	SRR14328022.fastq.gz	Fastqsanger.gz
	SRR14328023.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of dark-induced senescence of the leaves of Ran-GDP and Ran-GTP overexpression transgenic plants

Project description:Comparing transcriptome of the leaves of Ran-GDP and Ran-GTP overexpression transgenic plants before and after dark incubation, we discovered 851 differentially expressed genes that designated as Ran-regulated genes. The RNA-seq result confirmed the early senescence phenotype of Ran-GTP overexpression plants and the up-regulation of several signaling pathways, implied their positive roles in Ran-regulated senescence and suggest potential downstream targets of Ran. This study provided a mechanism that senescence process could be regulated by nuclear transportation machinery in Arabidopsis.

2021-04-27 | GSE173375 | GEO

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Project description:Circular RNAs (circRNAs), which can function as regulators of gene expression, are formed by back-splicing of precursor mRNAs in the nucleus. circRNAs are predominantly localized in the cytoplasm, indicating that they must be exported from the nucleus. Here, we uncover a pathway specific for nuclear export of circular RNA. This pathway requires Ran-GTP, Exportin-2 and IGF2BP1. Enhancing the nuclear Ran-GTP gradient by depletion or chemical inhibition of the major protein exporter, CRM1, selectively increases nuclear export of circRNAs, while reducing the nuclear Ran-GTP gradient selectively blocks circRNA export. Analysis of nuclear circRNA binding proteins reveals that interaction of IGF2BP1 with circRNA is enhanced by Ran-GTP, whereas its interaction with linear RNA is inhibited by Ran-GTP. Depletion or knockout of Exportin-2 specifically inhibits nuclear export of circRNA, while formation of an Exportin-2 circRNA export complex requires Ran-GTP and IGF2BP1. Our findings demonstrate that adaptors such as IGF2BP1 that bind directly to circular RNAs recruit Exportin-2 to export circRNAs in a mechanism analogous to protein export, rather than mRNA export.

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Nuclear export of circular RNA

Project description:Circular RNAs (circRNAs), which are increasingly being implicated in a variety of functions in normal and cancerous cells1-5, are formed by back-splicing of precursor mRNAs in the nucleus6-10. circRNAs are predom¬inantly localized in the cytoplasm, indicating that they must be exported from the nucleus. Here, we uncover a pathway specific for nuclear export of circular RNA. This pathway requires Ran-GTP, Exportin-2 and IGF2BP1. Enhancing the nuclear Ran-GTP gradient by depletion or chemical inhibition of the major protein exporter, CRM1, selectively increases nuclear export of circRNAs, while reducing the nuclear Ran-GTP gradient selectively blocks circRNA export. Depletion or knockout of Exportin-2 specifically inhibits nuclear export of circRNA. Analysis of nuclear circRNA binding proteins reveals that interaction of IGF2BP1 with circRNA is enhanced by Ran-GTP. Formation of circRNA export complexes in the nucleus is promoted by Ran-GTP through its interactions with IGF2BP1, Exportin-2 and circRNA. Our findings demonstrate that adaptors such as IGF2BP1 that bind directly to circular RNAs recruit Ran-GTP and Exportin-2 to export circRNAs in a mechanism analogous to protein export, rather than mRNA export.

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Project description:a proteomics strategy was performed to investigate the effects of different GTP/GDP imbalanced states on cellular function based on four established ARF6 cell models. Protein expression profiles were then generated by the label-free quantification (LFQ) method.

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RAN directly binds and stabilizes G3BP1 mRNA in the nucleus to facilitate proliferation and metastasis of nasopharyngeal carcinoma (si-RAN RNA-seq)

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