ArticleMolecular and cellular biology1998
The Drosophila gene for antizyme requires ribosomal frameshifting for expression and contains an intronic gene for snRNP Sm D3 on the opposite strand.
Article in Molecular and cellular biology, 1998. 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, 34 citations in OpenAlex.
- Biological Significance and Therapeutic Promise of Programmed Ribosomal Frameshifting.International journal of molecular sciences · 2025Review
- Phenotypic mutations contribute to protein diversity and shape protein evolution.Protein science : a publication of the Protein Society · 2022Review
- High frequency of +1 programmed ribosomal frameshifting in Euplotes octocarinatus.Scientific reports · 2016Article
- Gene Model Annotations for Drosophila melanogaster: The Rule-Benders.G3 (Bethesda, Md.) · 2015Article
- Revisiting the protein-coding gene catalog of Drosophila melanogaster using 12 fly genomes.Genome research · 2007Article
- Discovery of functional elements in 12 Drosophila genomes using evolutionary signatures.Nature · 2007Article
- Ribosomal frameshifting in decoding antizyme mRNAs from yeast and protists to humans: close to 300 cases reveal remarkable diversity despite underlying conservation.Nucleic acids research · 2007Review
- Functions of the nonsense-mediated mRNA decay pathway in Drosophila development.PLoS genetics · 2006Article
- Nonsense-mediated mRNA decay factors act in concert to regulate common mRNA targets.RNA (New York, N.Y.) · 2005Article
- Antizyme mRNA distribution and regulation in rat small intestinal enterocytes.Digestive diseases and sciences · 2002Article
- Article
- Purification of Drosophila snRNPs and characterization of two populations of functional U1 particles.RNA (New York, N.Y.) · 2001Article
- Mutations affecting the development of the peripheral nervous system in Drosophila: a molecular screen for novel proteins.Genetics · 2000Article
- Antizyme expression: a subversion of triplet decoding, which is remarkably conserved by evolution, is a sensor for an autoregulatory circuit.Nucleic acids research · 2000Review
- Discovery of a spermatogenesis stage-specific ornithine decarboxylase antizyme: antizyme 3.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Conservation of polyamine regulation by translational frameshifting from yeast to mammals.The EMBO journal · 2000Article
- Two zebrafish (Danio rerio) antizymes with different expression and activities.The Biochemical journal · 2000Article
- Identification of putative programmed -1 ribosomal frameshift signals in large DNA databases.Genome research · 1999Article
- Programmed frameshifting in the synthesis of mammalian antizyme is +1 in mammals, predominantly +1 in fission yeast, but -2 in budding yeast.RNA (New York, N.Y.) · 1998Article
- Does disparate occurrence of autoregulatory programmed frameshifting in decoding the release factor 2 gene reflect an ancient origin with loss in independent lineages?Journal of bacteriology · 1998Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Previously, a Drosophila melanogaster sequence with high homology to the sequence for mammalian antizyme (ornithine decarboxylase antizyme) was reported. The present study shows that homology of this coding sequence to its mammalian antizyme counterpart also extends to a 5' open reading frame (ORF) which encodes the amino-terminal part of antizyme and overlaps the +1 frame (ORF2) that encodes the carboxy-terminal three-quarters of the protein. Ribosomes shift frame from the 5' ORF to ORF2 with an efficiency regulated by polyamines. At least in mammals, this is part of an autoregulatory circuit. The shift site and 23 of 25 of the flanking nucleotides which are likely important for efficient frameshifting are identical to their mammalian homologs. In the reverse orientation, within one of the introns of the Drosophila antizyme gene, the gene for snRNP Sm D3 is located. Previously, it was shown that two closely linked P-element transposon insertions caused the gutfeeling phenotype of embryonic lethality and aberrant neuronal and muscle cell differentiation. The present work shows that defects in either snRNP Sm D3 or antizyme, or both, are likely causes of the phenotype.
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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.