ArticleNucleic acids research2024
Two-motif model illuminates DICER cleavage preferences.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- In silico unwinding ofRNA biology · 2026Article
- How Do DICER1 Syndrome Mutations Disrupt Catalysis? Unveiling Dicer Metal Binding Architecture and Mechanism of Action Using MD Simulations and QM/MM Calculations.Journal of computational chemistry · 2026Article
- Article
- miRNA dysregulation in depression: unraveling the interplay between neuroplasticity, HPA axis dysfunction, and neuroinflammation.Metabolic brain disease · 2025Review
- Key RNA elements influencing DCL1 cleavage in plant microRNA biogenesis.Nature plants · 2025Article
- A conserved RNA motif guides DCL1-mediated cleavage in plant microRNA biogenesis.Nature plants · 2025Article
- The biogenesis and regulation of animal microRNAs.Nature reviews. Molecular cell biology · 2025Review
- MirGeneDB 3.0: improved taxonomic sampling, uniform nomenclature of novel conserved microRNA families and updated covariance models.Nucleic acids research · 2025Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In humans, DICER is a key regulator of gene expression through its production of miRNAs and siRNAs by processing miRNA precursors (pre-miRNAs), short-hairpin RNAs (shRNAs), and long double-stranded RNAs (dsRNAs). To advance our understanding of this process, we employed high-throughput dicing assays using various shRNA variants and both wild-type and mutant DICER. Our analysis revealed that DICER predominantly cleaves shRNAs at two positions, specifically at 21 (DC21) and 22 (DC22) nucleotides from their 5'-end. Our investigation identified two different motifs, mWCU and YCR, that determine whether DICER cleaves at DC21 or DC22, depending on their locations in shRNAs/pre-miRNAs. These motifs can work together or independently to determine the cleavage sites of DICER. Furthermore, our findings indicate that dsRNA-binding domain (dsRBD) of DICER enhances its cleavage, and mWCU strengthens the interaction between dsRBD and RNA, leading to an even greater enhancement of the cleavage. Conversely, YCR functions independently of dsRBD. Our study proposes a two-motif model that sheds light on the intricate regulatory mechanisms involved in gene expression by elucidating how DICER recognizes its substrates, providing valuable insights into this critical biological process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.