ArticleGenetics2008
Mutations in the Drosophila mitochondrial tRNA amidotransferase, bene/gatA, cause growth defects in mitotic and endoreplicating tissues.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Transcriptomic Changes ofFrontiers in microbiology · 2022Article
- Knockout of Drosophila RNase ZL impairs mitochondrial transcript processing, respiration and cell cycle progression.Nucleic acids research · 2015Article
- Review
- Functional characterization of the Drosophila MRP (mitochondrial RNA processing) RNA gene.RNA (New York, N.Y.) · 2010Article
- Biogenesis of glutaminyl-mt tRNAGln in human mitochondria.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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Authors and funding
7 authors.
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Abstract
Rapid larval growth is essential in the development of most metazoans. In this article, we show that bene, a gene previously identified on the basis of its oogenesis defects, is also required for larval growth and viability. We show that all bene alleles disrupt gatA, which encodes the Drosophila homolog of glutamyl-tRNA(Gln) amidotransferase subunit A (GatA). bene alleles are now referred to as gatA. GatA proteins are highly conserved throughout eukaryotes and many prokaryotes. These enzymes are required for proper translation of the proteins encoded by the mitochondrial genome and by many eubacterial genomes. Mitotic and endoreplicating tissues in Drosophila gatA loss-of-function mutants grow slowly and never achieve wild-type size, and gatA larvae die before pupariation. gatA mutant eye clones exhibit growth and differentiation defects, indicating that gatA expression is required cell autonomously for normal growth. The gatA gene is widely expressed in mitotic and endoreplicating tissues.
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Registered trials
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