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 two organisms 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 complex
organization. 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.Comment: 22 pages, 4 figure
