The strongest form of synthetic rescues, in which the deleterious impact of a gene knockout is mitigated by an additional genetic perturbation that is also deleterious when considered in isolation, was modeled and predicted theoretically for gene interactions mediated by the metabolic network.
[4] Patient survival analysis was also shown to predict synthetic rescues and other types of interactions.
For example, a tRNA designated for the recognition of the codon TCA and the corresponding insertion of serine in the growing polypeptide chain can mutate so that it recognize a TAA stop codon and promote the insertion of serine instead of the termination of the polypeptide chain.
This could be particularly useful when a nonsense mutation (TCA >TAA) prevents the expression of a gene by either leading to a partially completed polypeptide or degradation of the mRNA by nonsense-mediated decay.
The redundancy of tRNA genes makes sure that such mutation would not prevent the normal insertion of serines when the TCA codon specifies them.