ArticleProceedings of the National Academy of Sciences of the United States of America2007
Buffering of deoxyribonucleotide pool homeostasis by threonine metabolism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Mechanistic insights on the mode of action of an antiproliferative thiosemicarbazone-nickel complex revealed by an integrated chemogenomic profiling study.Scientific reports · 2020Article
- Article
- A yeast phenomic model for the influence of Warburg metabolism on genetic buffering of doxorubicin.Cancer & metabolism · 2019Article
- Emerging Role of Precision Medicine in Cardiovascular Disease.Circulation research · 2018Review
- Role of Mitochondrial Retrograde Pathway in Regulating Ethanol-Inducible Filamentous Growth in Yeast.Frontiers in physiology · 2017Article
- Gene-nutrient interaction markedly influences yeast chronological lifespan.Experimental gerontology · 2016Article
- Analysis of 589,306 genomes identifies individuals resilient to severe Mendelian childhood diseases.Nature biotechnology · 2016Article
- Mitochondrial retrograde signaling inhibits the survival during prolong S/G2 arrest in Saccharomyces cerevisiae.Oncotarget · 2015Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Mitochondria to nucleus signaling and the role of ceramide in its integration into the suite of cell quality control processes during aging.Ageing research reviews · 2015Review
- Yeast Phenomics: An Experimental Approach for Modeling Gene Interaction Networks that Buffer Disease.Genes · 2015Article
- Aspartate facilitates mitochondrial function, growth arrest and survival during doxorubicin exposure.Cell cycle (Georgetown, Tex.) · 2015Article
- A metabolomics-based strategy for identification of gene targets for phenotype improvement and its application to 1-butanol tolerance in Saccharomyces cerevisiae.Biotechnology for biofuels · 2015Article
- Article
- Phenomic assessment of genetic buffering by kinetic analysis of cell arrays.Methods in molecular biology (Clifton, N.J.) · 2014Article
- DNA replication stress-induced loss of reproductive capacity in S. cerevisiae and its inhibition by caloric restriction.Cell cycle (Georgetown, Tex.) · 2013Article
- A yeast phenomic model for the gene interaction network modulating CFTR-ΔF508 protein biogenesis.Genome medicine · 2012Article
- Replication stress checkpoint signaling controls tRNA gene transcription.Nature structural & molecular biology · 2010Article
- Recursive expectation-maximization clustering: a method for identifying buffering mechanisms composed of phenomic modules.Chaos (Woodbury, N.Y.) · 2010Article
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1 author at 1 institution in 1 country.
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Abstract
Synergistically interacting gene mutations reveal buffering relationships that provide growth homeostasis through their compensation of one another. This analysis in Saccharomyces cerevisiae revealed genetic modules involved in tricarboxylic acid cycle regulation (RTG1, RTG2, RTG3), threonine biosynthesis (HOM3, HOM2, HOM6, THR1, THR4), amino acid permease trafficking (LST4, LST7), and threonine catabolism (GLY1). These modules contribute to a molecular circuit that regulates threonine metabolism and buffers deficiency in deoxyribonucleotide biosynthesis. Phenotypic, genetic, and biochemical evidence for this buffering circuit was obtained through analysis of deletion mutants, titratable alleles of ribonucleotide reductase genes, and measurements of intracellular deoxyribonucleotide pool concentrations. This circuit provides experimental evidence, in eukaryotes, for the presence of a high-flux backbone of metabolism, which was previously predicted from in silico modeling of global metabolism in bacteria. This part of the high-flux backbone appears to buffer deficiency in ribonucleotide reductase by enabling a compensatory increase in de novo purine biosynthesis that provides additional rate-limiting substrates for dNTP production and DNA synthesis. Hypotheses regarding unexpected connections between these metabolic pathways were facilitated by genome-wide but also highly quantitative phenotypic assessment of interactions. Validation of these hypotheses substantiates the added benefit of quantitative phenotyping for identifying subtleties in gene interaction networks that modulate cellular phenotypes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.