ArticleScientific reports2012
Predicting effects of structural stress in a genome-reduced model bacterial metabolism.
Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Metabolic plasticity in synthetic lethal mutants: Viability at higher cost.PLoS computational biology · 2018Article
- Essential plasticity and redundancy of metabolism unveiled by synthetic lethality analysis.PLoS computational biology · 2014Article
- Article
- Dissecting the energy metabolism in Mycoplasma pneumoniae through genome-scale metabolic modeling.Molecular systems biology · 2013Article
- Mycoplasmas and Their Antibiotic Resistance: The Problems and Prospects in Controlling Infections.Acta naturaeArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycoplasma pneumoniae is a human pathogen recently proposed as a genome-reduced model for bacterial systems biology. Here, we study the response of its metabolic network to different forms of structural stress, including removal of individual and pairs of reactions and knockout of genes and clusters of co-expressed genes. Our results reveal a network architecture as robust as that of other model bacteria regarding multiple failures, although less robust against individual reaction inactivation. Interestingly, metabolite motifs associated to reactions can predict the propagation of inactivation cascades and damage amplification effects arising in double knockouts. We also detect a significant correlation between gene essentiality and damages produced by single gene knockouts, and find that genes controlling high-damage reactions tend to be expressed independently of each other, a functional switch mechanism that, simultaneously, acts as a genetic firewall to protect metabolism. Prediction of failure propagation is crucial for metabolic engineering or disease treatment.
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Registered trials
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