ArticleThe Plant cell2024
Evidence for an RNAi-independent role of Arabidopsis DICER-LIKE2 in growth inhibition and basal antiviral resistance.
Article in The Plant cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Haplotype-phased 'Ottawa 3' genome unravels differential reaction of apple rootstock roots to mixed viral infection.The Plant journal : for cell and molecular biology · 2026Article
- Molecular basis of plant DCL4 action that outcompetes DCL2.Nature plants · 2026Article
- Coding Transcript-Derived Small Interfering RNAs: Their Biogenesis and Molecular Function in Arabidopsis.International journal of molecular sciences · 2026Review
- The action of Arabidopsis DICER-LIKE 2 in plant growth inhibition.The Plant cell · 2025Article
- Response to "The action of Arabidopsis DICER-LIKE2 in plant growth inhibition".The Plant cell · 2025Article
- Atypical epigenetic and small RNA control of degenerated transposons and their fragments in clonally reproducingGenome research · 2025Article
- Small Interfering RNAs as Critical Regulators of Plant Life Process: New Perspectives on Regulating the Transcriptomic Machinery.International journal of molecular sciences · 2025Review
- The biogenesis, regulation and functions of transitive siRNA in plants.Acta biochimica et biophysica Sinica · 2024Review
- Dicing DICER-LIKE2 roles: Identification of siRNA-independent DICER-LIKE2 functions.The Plant cell · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Flowering plant genomes encode four or five DICER-LIKE (DCL) enzymes that produce small interfering RNAs (siRNAs) and microRNAs, which function in RNA interference (RNAi). Different RNAi pathways in plants effect transposon silencing, antiviral defense, and endogenous gene regulation. DCL2 acts genetically redundantly with DCL4 to confer basal antiviral defense. However, DCL2 may also counteract DCL4 since knockout of DCL4 causes growth defects that are suppressed by DCL2 inactivation. Current models maintain that RNAi via DCL2-dependent siRNAs is the biochemical basis of both effects. Here, we report that DCL2-mediated antiviral resistance and growth defects cannot be explained by the silencing effects of DCL2-dependent siRNAs. Both functions are defective in genetic backgrounds that maintain high levels of DCL2-dependent siRNAs, either with specific point mutations in DCL2 or with reduced DCL2 dosage because of heterozygosity for dcl2 knockout alleles. Intriguingly, all DCL2 functions require its catalytic activity, and the penetrance of DCL2-dependent growth phenotypes in dcl4 mutants correlates with DCL2 protein levels but not with levels of major DCL2-dependent siRNAs. We discuss this requirement and correlation with catalytic activity but not with resulting siRNAs, in light of other findings that reveal a DCL2 function in innate immunity activation triggered by cytoplasmic double-stranded RNA.
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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.