We unravel how functional plasticity and redundancy are essential mechanisms underlying the ability to survive of metabolic networks. For that, we perform an exhaustive computational screening of synthetic lethal reaction pairs in Escherichia coli in  minimal medium and  find that synthetic lethals divide in two different groups depending on whether the synthetic lethal interaction works as a back up or as a parallel use mechanism, the first corresponding to essential plasticity and the second to essential redundancy. In E. coli, the analysis of how pathways are entangled through essential redundancy supports the view that synthetic lethality affects preferentially a single function or pathway. In contrast, essential plasticity, the dominant class, tends to be inter-pathway but concentrated and unveils Cell Envelope Biosynthesis as an essential backup to Membrane Lipid Metabolism. When comparing E. coli and Mycoplasma pneumoniae, we find that the metabolic networks of the URLanisms exhibit opposite relationships between the relative importance of plasticity and redundancy , consistent with the conjecture that plasticity is a more sophisticated mechanism that requires a more URLanization. Finally, coessential reaction pairs are explored in different environmental conditions to uncover the interplay between the two mechanisms. We find that synthetic lethal interactions and their classification in plasticity and redundancy are basically insensitive to minimal medium composition, and are highly conserved even when the environment is enriched with nonessential compounds or overconstrained to decrease maximum biomass formation.
We unravel how functional plasticity and redundancy are essential mechanisms underlying the ability to survive of metabolic networks. We perform an exhaustive computational screening of synthetic lethal reaction pairs in Escherichia coli in a minimal medium and we find that synthetic lethal pairs divide in two different groups depending on whether the synthetic lethal interaction works as a backup or as a parallel use mechanism, the first corresponding to essential plasticity and the second to essential redundancy. In E. coli, the analysis of pathways entanglement through essential redundancy supports the view that synthetic lethality affects preferentially a single function or pathway. In contrast, essential plasticity, the dominant class, tends to be inter-pathway but strongly localized and unveils Cell Envelope Biosynthesis as an essential backup for Membrane Lipid Metabolism. When comparing E. coli and Mycoplasma pneumoniae, we find that the metabolic networks of the URLanisms exhibit a large difference in the relative importance of plasticity and redundancy which is consistent with the conjecture that plasticity is a sophisticated mechanism that requires a URLanization. Finally, coessential reaction pairs are explored in different environmental conditions to uncover the interplay between the two mechanisms. We find that synthetic lethal interactions and their classification in plasticity and redundancy are basically insensitive to medium composition, and are highly conserved even when the environment is enriched with nonessential compounds or overconstrained to decrease maximum biomass formation.
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For that, we
We
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a
A
we
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lethals
lethal pairs
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back up
backup
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how pathways are entangled
pathways entanglement
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concentrated
strongly localized
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to
for
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opposite relationships between
a large difference in
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,
which is
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more
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more
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minimal