Abstract
Protein-protein interaction (PPI) networks represent complex intra-cellular protein interactions, and the presence or absence of such interactions can lead to biological changes in an organism. Recent network-based approaches have shown that a phenotype9s PPI network9s resilience to environmental perturbations is related to its placement in the tree of life; though we still do not know how or why certain intra-cellular factors can bring about this resilience. One such factor is gene expression, which controls the simultaneous presence of proteins for allowed extant interactions and the possibility of novel associations. Here, we explore the influence of gene expression and network properties on a PPI network9s resilience, focusing especially on ribosomal proteins---vital molecular-complexes involved in protein synthesis, which have been extensively and reliably mapped in many species. Using publicly-available data of ribosomal PPIs for E. coli , S.cerevisae , and H. sapiens , we compute changes in network resilience as new nodes (proteins) are added to the networks under three node addition mechanisms---random, degree-based, and gene-expression-based attachments. By calculating the resilience of the resulting networks, we estimate the effectiveness of these node addition mechanisms. We demonstrate that adding nodes with gene-expression-based preferential attachment (as opposed to random or degree-based) preserves and can increase the original resilience of PPI network. This holds in all three species regardless of their distributions of gene expressions or their network community structure. These findings introduce a general notion of prospective resilience , which highlights the key role of network structures in understanding the evolvability of phenotypic traits.