ArticlePloS one2012
Suppressor analyses identify threonine as a modulator of ridA mutant phenotypes in Salmonella enterica.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- PLP Homeostasis Protein Is Required for Efficient Maturation of Aromatic Amino Acid Aminotransferase in Salmonella enterica.Molecular microbiology · 2026Article
- Perturbation of the MetJ regulon impacts the consequences of 2-aminoacrylate stress inMicrobiology (Reading, England) · 2025Article
- Tetrahydrofolate levels influence 2-aminoacrylate stress inJournal of bacteriology · 2024Article
- RidA proteins contribute to fitness ofMicrobial cell (Graz, Austria) · 2024Article
- Modulators of a robust and efficient metabolism: Perspective and insights from the Rid superfamily of proteins.Advances in microbial physiology · 2023Review
- Article
- Absence of MMF1 disrupts heme biosynthesis by targeting Hem1pin Saccharomyces cerevisiae.Yeast (Chichester, England) · 2021Article
- RidA Proteins Protect against Metabolic Damage by Reactive Intermediates.Microbiology and molecular biology reviews : MMBR · 2020Review
- Reactive Enamines and Imines In Vivo: Lessons from the RidA Paradigm.Trends in biochemical sciences · 2019Review
- Analyses of variants of the Ser/Thr dehydratase IlvA provide insight into 2-aminoacrylate metabolism inThe Journal of biological chemistry · 2018Article
- Expression of Pyridoxal 5'-Phosphate-Independent Racemases Can Reduce 2-Aminoacrylate Stress in Salmonella enterica.Journal of bacteriology · 2018Article
- Article
- Endogenously generated 2-aminoacrylate inhibits motility in Salmonella enterica.Scientific reports · 2017Article
- The Response to 2-Aminoacrylate Differs in Escherichia coli and Salmonella enterica, despite Shared Metabolic Components.Journal of bacteriology · 2017Article
- 2-Aminoacrylate Stress Induces a Context-Dependent Glycine Requirement in ridA Strains of Salmonella enterica.Journal of bacteriology · 2016Article
- From microbiology to cancer biology: the Rid protein family prevents cellular damage caused by endogenously generated reactive nitrogen species.Molecular microbiology · 2015Review
- Endogenous synthesis of 2-aminoacrylate contributes to cysteine sensitivity in Salmonella enterica.Journal of bacteriology · 2014Article
- Arabidopsis and maize RidA proteins preempt reactive enamine/imine damage to branched-chain amino acid biosynthesis in plastids.The Plant cell · 2014Article
- Decreased coenzyme A levels in ridA mutant strains of Salmonella enterica result from inactivated serine hydroxymethyltransferase.Molecular microbiology · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The RidA (YjgF/YER057c/UK114) family of proteins is broadly conserved in the three domains of life yet the functional understanding of these proteins is at an early stage. Physiological studies of ridA mutant strains of Salmonella enterica provided a framework to inform in vitro studies and led to the description of a conserved biochemical activity for this family. ridA mutant strains of S. enterica have characteristic phenotypes including new synthesis of thiamine biosynthetic intermediate phosphoribosylamine (PRA), inability to grow on pyruvate as a sole carbon and energy source or when serine is present in the minimal growth medium, and a decreased specific activity of transaminase B (IlvE). Secondary mutations restoring growth to a ridA mutant in the presence of serine were in dapA (encoding dihydrodipicolinate synthase) and thrA (encoding homoserine dehydrogenase). These mutations suppressed multiple ridA mutant phenotypes by increasing the synthesis of threonine. The ability of threonine to suppress the metabolic defects of a ridA mutant is discussed in the context of recent biochemical data and in vivo results presented here.
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