Cellular responses to reactive oxygen species are predicted from molecular mechanisms.
Proc Natl Acad Sci U S A
; 116(28): 14368-14373, 2019 07 09.
Article
em En
| MEDLINE
| ID: mdl-31270234
ABSTRACT
Catalysis using iron-sulfur clusters and transition metals can be traced back to the last universal common ancestor. The damage to metalloproteins caused by reactive oxygen species (ROS) can prevent cell growth and survival when unmanaged, thus eliciting an essential stress response that is universal and fundamental in biology. Here we develop a computable multiscale description of the ROS stress response in Escherichia coli, called OxidizeME. We use OxidizeME to explain four key responses to oxidative stress 1) ROS-induced auxotrophy for branched-chain, aromatic, and sulfurous amino acids; 2) nutrient-dependent sensitivity of growth rate to ROS; 3) ROS-specific differential gene expression separate from global growth-associated differential expression; and 4) coordinated expression of iron-sulfur cluster (ISC) and sulfur assimilation (SUF) systems for iron-sulfur cluster biosynthesis. These results show that we can now develop fundamental and quantitative genotype-phenotype relationships for stress responses on a genome-wide basis.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Espécies Reativas de Oxigênio
/
Ferro
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Proteínas Ferro-Enxofre
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Metaloproteínas
Tipo de estudo:
Prognostic_studies
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Risk_factors_studies
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article