Evidence map›Paper›PMID 32833957›Full record

ArticlePLoS biology2020

Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect.

Robin Green, Sonal, Lin Wang, Samuel F M Hart, Wenyun Lu, David Skelding, Justin C Burton, Hanbing Mi, Aric Capel, Hung Alex Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 24 citations in OpenAlex.

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  5. Evolutionary repeatability of emergent properties of ecological communities.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Robin GreenDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0001-7411-0593
SonalDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0002-2361-4131
Lin WangDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.ORCID 0000-0002-9370-6891
Samuel F M HartDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0002-5068-2199
Wenyun LuDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.
David SkeldingDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Justin C BurtonDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0002-4797-8968
Hanbing MiDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Aric CapelDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0002-2748-379X
Hung Alex ChenDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0001-5119-6208
Aaron LinDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0002-6006-0908
Arvind R SubramaniamDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Joshua D RabinowitzDepartment of Chemistry and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey, United States of America.ORCID 0000-0002-1247-4727
Wenying ShouDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.ORCID 0000-0001-5693-381X
Fred Hutch Cancer Center · USPrinceton University · US

Funding

Regulation of Protein Synthesis by Synonymous Codon UsageR35GM119835 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SUBRAMANIAM, ARVIND RASI · 2016 to 2025
$4.1M
Cellular Cooperation and Cheating: an Experimental and Mathematical AnalysisDP2OD006498 · OD · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SHOU, WENYING · 2009 to 2009
$2.6M
Understanding Robustness of a Cooperative Microbial Community during EvolutionR01GM124128 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI XIE, LI · 2017 to 2020
$1.4M
Revealing cancer metabolism via mass spectrometry and isotope tracersR50CA211437 · NCI · PRINCETON UNIVERSITY · PI Wenyun Lu · 2016 to 2026
$1.3M
Biotechnology and Biological Sciences Research Council 1917258NCI NIH HHS R50 CA211437NIGMS NIH HHS R01 GM124128NIGMS NIH HHS R35 GM119835NIH HHS DP2 OD006498
6 · The paper itself

Abstract

In eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability. Overactive growth during nutrient limitation ("nutrient-growth dysregulation") can lead to rapid cell death. Here, we demonstrate that cells can adapt to nutrient-growth dysregulation by evolving major metabolic defects. Specifically, when yeast lysine-auxotrophic mutant lys- encountered lysine limitation, an evolutionarily novel stress, cells suffered nutrient-growth dysregulation. A subpopulation repeatedly evolved to lose the ability to synthesize organosulfurs (lys-orgS-). Organosulfurs, mainly reduced glutathione (GSH) and GSH conjugates, were released by lys- cells during lysine limitation when growth was dysregulated, but not during glucose limitation when growth was regulated. Limiting organosulfurs conferred a frequency-dependent fitness advantage to lys-orgS- by eliciting a proper slow growth program, including autophagy. Thus, nutrient-growth dysregulation is associated with rapid organosulfur release, which enables the selection of organosulfur auxotrophy to better tune cell growth to the metabolic environment. We speculate that evolutionarily novel stresses can trigger atypical release of certain metabolites, setting the stage for the evolution of new ecological interactions.

Indexed as

Adaptation, PhysiologicalAutophagyBiological EvolutionGlucoseLysineMetabolic Networks and PathwaysNitrogenNutrientsRibosomesSaccharomyces cerevisiaeSirolimusStress, PhysiologicalGlucoseLysineNitrogenNutrientsSirolimus

Identifiers

PMID32833957
PMCPMC7470746
OpenAlexW3081337239

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.