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NRDE2 interacts with transcription-associated and splicing factors and modulates gene expression and splicing

ABSTRACT: To investigate the function of Nuclear RNAi-Defective 2 (NRDE2) in gene expression, we performed RNA-seq following its transient knock-down. Differential expression analysis showed that loss of NRDE2 modulated the expression of thousands of genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE300903 | GEO | 2025/11/21

REPOSITORIES: GEO

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NRDE2 negatively regulates nuclear exosome functions II

Project description:To examine whether NRDE2 can impact the competition between hMTR4 and ALYREF, we performed stranded RNA-seq to detect nuclear RNAs isolated from NRDE2 and control knockdown cells.

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NRDE2 negatively regulates nuclear exosome functions I

Project description:To examine whether NRDE2 can impact the competition between hMTR4 and ALYREF, we performed stranded RNA-seq to detect total RNAs isolated from NRDE2 and control knockdown cells.

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NRDE2 negatively regulates nuclear exosome functions IV

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RNA-seq analysis of control and NRDE2-depleted breast cancer cells

Project description:Purpose: investigate transcriptomic changes following depletion of the NRDE2 gene Methods: MDA-MB-231 breast cancer cells were transfected with 20nM control or NRDE2-targeting siRNAs, and RNA was collected after 48h for RNA-seq analysis Results: We analyzed si-Control and si-NRDE2-treated samples in triplicate (~46-64 million reads per sample) and find that the near-complete loss of NRDE2 results in generally modest changes in gene expression, with only 84 genes deregulated >2-fold. We also identify 342 introns which are differentially retained in NRDE2-depleted cells. Conclusions: NRDE2 is required for suppressing intron retention in a subset of genes

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NRDE2 negatively regulates nuclear exosome functions

Project description:The exosome functions in the degradation of diverse RNA species, yet how it is negatively regulated remains largely unknown. Here, we show that NRDE2 forms a 1:1 complex with MTR4, a nuclear exosome cofactor critical for exosome recruitment, via a conserved MTR4-interacting domain (MID). Unexpectedly, NRDE2 mainly localizes in nuclear speckles, where it inhibits MTR4 recruitment and RNA degradation, and thereby ensures efficient mRNA nuclear export. Structural and biochemical data revealed that NRDE2 interacts with MTR4's key residues, locks MTR4 in a closed conformation, and inhibits MTR4 interaction with the exosome as well as proteins important for MTR4 recruitment, such as the cap-binding complex (CBC) and ZFC3H1. Functionally, MID deletion results in the loss of self-renewal of mouse embryonic stem cells. Together, our data pinpoint NRDE2 as a nuclear exosome negative regulator that ensures mRNA stability and nuclear export.

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Deep sequencing of NPKO-1 cells with NRDE2 knockdown

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NRDE2 acts as a negative regulator of the exosome complex by disrupting hMTR4 interactome

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NRDE2 negatively regulates nuclear exosome functions

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Novel RNA-binding Proteins Bind U1 snRNA to Promote Splicing of Weak 5' Splice Sites

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NRDE2 negatively regulates nuclear exosome functions I

Project description:NRDE2 negatively regulates nuclear exosome functions I

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