Cellular tensegrity is a model for cell architecture in which microfilaments and intermediate filaments bear tensional forces and these are balanced by elements that resist compression, such as microtubules and matrix adhesions. In part II of a two-part Commentary on the subject, Donald Ingber discusses how tensegrity architecture might provide a basis for biocomplexity by allowing cells to integrate chemical and physical signals into a network from which complex behaviours can emerge (see ). Several studies indicate that mechanical stress applied to integrins at the cell surface can induce cytoskeletal reorganization, signal transduction and gene expression. Moreover, at the whole cell level, cell shape distortion is able to switch cells between gene programmes that lead to distinct cell fates – growth,differentiation or apoptosis – and alterations in cytoskeletal pre-stress (a critical parameter in cellular tensegrity) have been shown to influence tissue patterning. Ingber suggests that tensegrity thus represents the hardware behind living systems, the signalling machinery being the software. In the context of this dynamic information-processing network, he proposes that cell fates can be viewed as `attractors' – stable states whose formation is an emergent property of the network.
