(504f) Cascading Failure in Metabolic Networks: Searching for Links Between Form and Function

Metabolism is an ideal prototype for evolvable, adaptable complex systems ? the explosion of high throughput technologies in genomics yielded near-complete knowledge of its function while the almost simultaneous emergence of complex networks theory produced comparable advances in our ability to deconstruct its architecture. Still, bridging function with form remains an ongoing challenge. Here we use a topological flux balance model to describe the cascading effect of reaction failures in metabolic networks. Several form-function questions naturally follow: Is the distribution of failure events power law, as seen in other complex networks (e.g., the electric grid, or the classic forest fire paradigm)? Does it reflect a particularly robust and/or fragile metabolic architecture? Some of these questions are addressed by computational techniques ? we show, via null model comparison, that metabolic architecture is especially robust (this robustness is not explained by degree distribution, as had been an early claim). Surprisingly, however, the frequency of ?uniquely produced-uniquely consumed? metabolite clusters is nearly identical to the null model. Additional insight is gained from theoretical analysis ? mapping the cascading failure algorithm onto a percolation model, we show that the null model is super-critical, suggesting that structural motifs in metabolic networks act crucially to prevent network-spanning failures.