Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2
ABSTRACTAmino acyl-tRNA synthetases perform diverse non-canonical functions aside from their essential role in charging tRNAs with their cognate amino acid. The phenylalanyl-tRNA synthetase (PheRS/FARS) is an α2β2 tetramer that is needed for charging the tRNAPhe for its translation activity. Fragmen...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2024-12-01
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Series: | Fly |
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Online Access: | https://www.tandfonline.com/doi/10.1080/19336934.2024.2308737 |
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author | Dominique Brunßen Beat Suter |
author_facet | Dominique Brunßen Beat Suter |
author_sort | Dominique Brunßen |
collection | DOAJ |
description | ABSTRACTAmino acyl-tRNA synthetases perform diverse non-canonical functions aside from their essential role in charging tRNAs with their cognate amino acid. The phenylalanyl-tRNA synthetase (PheRS/FARS) is an α2β2 tetramer that is needed for charging the tRNAPhe for its translation activity. Fragments of the α-subunit have been shown to display an additional, translation-independent, function that activates growth and proliferation and counteracts Notch signalling. Here we show in Drosophila that overexpressing the β-subunit in the context of the complete PheRS leads to larval roaming, food avoidance, slow growth, and a developmental delay that can last several days and even prevents pupation. These behavioural and developmental phenotypes are induced by PheRS expression in CCHa2+ and Pros+ cells. Simultaneous expression of β-PheRS, α-PheRS, and the appetite-inducing CCHa2 peptide rescued these phenotypes, linking this β-PheRS activity to the appetite-controlling pathway. The fragmentation dynamic of the excessive β-PheRS points to β-PheRS fragments as possible candidate inducers of these phenotypes. Because fragmentation of human FARS has also been observed in human cells and mutations in human β-PheRS (FARSB) can lead to problems in gaining weight, Drosophila β-PheRS can also serve as a model for the human phenotype and possibly also for obesity. |
first_indexed | 2024-03-07T23:36:57Z |
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id | doaj.art-fb1f563512584e86ab495f7cdf8d46e4 |
institution | Directory Open Access Journal |
issn | 1933-6934 1933-6942 |
language | English |
last_indexed | 2024-03-07T23:36:57Z |
publishDate | 2024-12-01 |
publisher | Taylor & Francis Group |
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series | Fly |
spelling | doaj.art-fb1f563512584e86ab495f7cdf8d46e42024-02-20T06:49:22ZengTaylor & Francis GroupFly1933-69341933-69422024-12-0118110.1080/19336934.2024.2308737Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2Dominique Brunßen0Beat Suter1Institute of Cell Biology, University of Bern, Bern, SwitzerlandInstitute of Cell Biology, University of Bern, Bern, SwitzerlandABSTRACTAmino acyl-tRNA synthetases perform diverse non-canonical functions aside from their essential role in charging tRNAs with their cognate amino acid. The phenylalanyl-tRNA synthetase (PheRS/FARS) is an α2β2 tetramer that is needed for charging the tRNAPhe for its translation activity. Fragments of the α-subunit have been shown to display an additional, translation-independent, function that activates growth and proliferation and counteracts Notch signalling. Here we show in Drosophila that overexpressing the β-subunit in the context of the complete PheRS leads to larval roaming, food avoidance, slow growth, and a developmental delay that can last several days and even prevents pupation. These behavioural and developmental phenotypes are induced by PheRS expression in CCHa2+ and Pros+ cells. Simultaneous expression of β-PheRS, α-PheRS, and the appetite-inducing CCHa2 peptide rescued these phenotypes, linking this β-PheRS activity to the appetite-controlling pathway. The fragmentation dynamic of the excessive β-PheRS points to β-PheRS fragments as possible candidate inducers of these phenotypes. Because fragmentation of human FARS has also been observed in human cells and mutations in human β-PheRS (FARSB) can lead to problems in gaining weight, Drosophila β-PheRS can also serve as a model for the human phenotype and possibly also for obesity.https://www.tandfonline.com/doi/10.1080/19336934.2024.2308737Drosophiladevelopmental delaygrowthroamingsatiety signaling |
spellingShingle | Dominique Brunßen Beat Suter Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 Fly Drosophila developmental delay growth roaming satiety signaling |
title | Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 |
title_full | Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 |
title_fullStr | Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 |
title_full_unstemmed | Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 |
title_short | Effects of unstable β-PheRS on food avoidance, growth, and development are suppressed by the appetite hormone CCHa2 |
title_sort | effects of unstable β phers on food avoidance growth and development are suppressed by the appetite hormone ccha2 |
topic | Drosophila developmental delay growth roaming satiety signaling |
url | https://www.tandfonline.com/doi/10.1080/19336934.2024.2308737 |
work_keys_str_mv | AT dominiquebrunßen effectsofunstablebphersonfoodavoidancegrowthanddevelopmentaresuppressedbytheappetitehormoneccha2 AT beatsuter effectsofunstablebphersonfoodavoidancegrowthanddevelopmentaresuppressedbytheappetitehormoneccha2 |