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  , the first corresponding to essential plasticity and the second to essential redundancy. In E. coli, the analysis of how pathways are entangled through essential plasticity and redundancy supports the view that synthetic lethality affects preferentially a single function or pathway , although with a major exception which unveils Cell Envelope Biosysthesis 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  .
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 .
A
mechanism
D
plasticity and
R
, although with a major exception which
. In contrast, essential plasticity, the dominant class, tends to be inter-pathway but concentrated and
R
Biosysthesis
Biosynthesis
A
or overconstrained to decrease maximum biomass formation