ArticlePloS one2013
Validating RNAi phenotypes in Drosophila using a synthetic RNAi-resistant transgene.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Knockdown of PR-DUB subunit calypso in the developing Drosophila eye and wing results in mis-patterned tissues with altered size and shape.G3 (Bethesda, Md.) · 2025Article
- Formin 3 directs dendritic architecture via microtubule regulation and is required for somatosensory nociceptive behavior.Development (Cambridge, England) · 2021Article
- Drosophila USP22/nonstop polarizes the actin cytoskeleton during collective border cell migration.The Journal of cell biology · 2021Article
- Functional interplay between long non-coding RNAs and the Wnt signaling cascade in osteosarcoma.Cancer cell international · 2021Review
- Reverse-genetics studies of lncRNAs-what we have learnt and paths forward.Genome biology · 2020Review
- A CRISPR/Cas13-based approach demonstrates biological relevance of vlinc class of long non-coding RNAs in anticancer drug response.Scientific reports · 2020Article
- Transcriptional responses to hyperplastic MRL signalling in Drosophila.Open biology · 2017Article
- Analyzing the roles of multi-functional proteins in cells: The case of arrestins and GRKs.Critical reviews in biochemistry and molecular biology · 2015Review
- RNAi screening in Drosophila cells and in vivo.Methods (San Diego, Calif.) · 2014Review
- Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo.The Journal of cell biology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
RNA interference (RNAi) is a powerful and widely used approach to investigate gene function, but a major limitation of the approach is the high incidence of non-specific phenotypes that arise due to off-target effects. We previously showed that RNAi-mediated knock-down of pico, which encodes the only member of the MRL family of adapter proteins in Drosophila, resulted in reduction in cell number and size leading to reduced tissue growth. In contrast, a recent study reported that pico knockdown leads to tissue dysmorphology, pointing to an indirect role for pico in the control of wing size. To understand the cause of this disparity we have utilised a synthetic RNAi-resistant transgene, which bears minimal sequence homology to the predicted dsRNA but encodes wild type Pico protein, to reanalyse the RNAi lines used in the two studies. We find that the RNAi lines from different sources exhibit different effects, with one set of lines uniquely resulting in a tissue dysmorphology phenotype when expressed in the developing wing. Importantly, the loss of tissue morphology fails to be complemented by co-overexpression of RNAi-resistant pico suggesting that this phenotype is the result of an off-target effect. This highlights the importance of careful validation of RNAi-induced phenotypes, and shows the potential of synthetic transgenes for their experimental validation.
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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.