ArticleYeast (Chichester, England)2016
Tryptophan biosynthesis is important for resistance to replicative stress in Saccharomyces cerevisiae.
Article in Yeast (Chichester, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- A comprehensive review and comparison of L-tryptophan biosynthesis inFrontiers in bioengineering and biotechnology · 2023Review
- RNA-Seq Based Transcriptome Analysis ofJournal of fungi (Basel, Switzerland) · 2022Article
- The Shu complex prevents mutagenesis and cytotoxicity of single-strand specific alkylation lesions.eLife · 2021Article
- Differential proteomic analysis by SWATH-MS unravels the most dominant mechanisms underlying yeast adaptation to non-optimal temperatures under anaerobic conditions.Scientific reports · 2020Article
- Oxidative Stress Responses and Nutrient Starvation in MCHM TreatedG3 (Bethesda, Md.) · 2020Article
- Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.PloS one · 2019Article
- Cdk1-interacting protein Cip1 is regulated by the S phase checkpoint in response to genotoxic stress.Genes to cells : devoted to molecular & cellular mechanisms · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Acute tryptophan depletion is used to induce low levels of serotonin in the brain. This method has been widely used in psychiatric studies to evaluate the effect of low levels of serotonin, and is generally considered a safe and reversible procedure. Here we use the budding yeast Saccharomyces cerevisiae to study the effects of tryptophan depletion on growth rate upon exposure to DNA-damaging agents. Surprisingly, we found that budding yeast undergoing tryptophan depletion were more sensitive to DNA-damaging agents such as methyl methanesulphonate (MMS) and hydroxyurea (HU). We found that this defect was independent of several DNA repair pathways, such as homologous recombination, base excision repair and translesion synthesis, and that this damage sensitivity was not due to impaired S-phase signalling. Upon further analysis, we found that the DNA-damage sensitivity of tryptophan depletion was likely due to impaired protein synthesis. These studies describe an important source of variance in budding yeast when using tryptophan as an auxotrophic marker, particularly on studies focusing on DNA repair, and suggest that further testing of the effect of tryptophan depletion on DNA repair in mammalian cells is warranted. Copyright © 2016 John Wiley & Sons, Ltd.
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