ArticleGenetics2003
Mutations in eukaryotic release factors 1 and 3 act as general nonsense suppressors in Drosophila.
Article in Genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Tissue-specific regulation of translational readthrough tunes functions of the traffic jam transcription factor.Nucleic acids research · 2022Article
- Article
- Yeast applied readthrough inducing system (YARIS): an invivo assay for the comprehensive study of translational readthrough.Nucleic acids research · 2019Article
- Toward a Kinetic Understanding of Eukaryotic Translation.Cold Spring Harbor perspectives in biology · 2019Review
- An Unexpected Regulatory Cascade Governs a Core Function of the Drosophila PRC1 Chromatin Protein Su(z)2.Genetics · 2017Article
- Article
- A system for coordinated analysis of translational readthrough and nonsense-mediated mRNA decay.PloS one · 2017Article
- Hydroxylation and translational adaptation to stress: some answers lie beyond the STOP codon.Cellular and molecular life sciences : CMLS · 2016Review
- Translation initiation factor eIF3 promotes programmed stop codon readthrough.Nucleic acids research · 2015Article
- Nonsense codon suppression in fission yeast due to mutations of tRNA(Ser.11) and translation release factor Sup35 (eRF3).Current genetics · 2015Article
- Ribosome profiling reveals pervasive and regulated stop codon readthrough in Drosophila melanogaster.eLife · 2013Article
- The Drosophila over compensating males gene genetically inhibits dosage compensation in males.PloS one · 2013Article
- Evidence of abundant stop codon readthrough in Drosophila and other metazoa.Genome research · 2011Article
- Evolution of molecular error rates and the consequences for evolvability.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Cell cycle arrest by a gradient of Dpp signaling during Drosophila eye development.BMC developmental biology · 2010Article
- Genetic evidence that Drosophila frizzled controls planar cell polarity and Armadillo signaling by a common mechanism.Genetics · 2005Article
- RacGap50C negatively regulates wingless pathway activity during Drosophila embryonic development.Genetics · 2005Article
- The Drosophila U1-70K protein is required for viability, but its arginine-rich domain is dispensable.Genetics · 2004Article
- The effect of eukaryotic release factor depletion on translation termination in human cell lines.Nucleic acids research · 2004Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In a screen for suppressors of the Drosophila wingless(PE4) nonsense allele, we isolated mutations in the two components that form eukaryotic release factor. eRF1 and eRF3 comprise the translation termination complex that recognizes stop codons and catalyzes the release of nascent polypeptide chains from ribosomes. Mutations disrupting the Drosophila eRF1 and eRF3 show a strong maternal-effect nonsense suppression due to readthrough of stop codons and are zygotically lethal during larval stages. We tested nonsense mutations in wg and in other embryonically acting genes and found that different stop codons can be suppressed but only a subset of nonsense alleles are subject to suppression. We suspect that the context of the stop codon is significant: nonsense alleles sensitive to suppression by eRF1 and eRF3 encode stop codons that are immediately followed by a cytidine. Such suppressible alleles appear to be intrinsically weak, with a low level of readthrough that is enhanced when translation termination is disrupted. Thus the eRF1 and eRF3 mutations provide a tool for identifying nonsense alleles that are leaky. Our findings have important implications for assigning null mutant phenotypes and for selecting appropriate alleles to use in suppressor screens.
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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.