Gene duplicates have the inherent property of initially being functionally redundant. This means that they can compensate for the effect of deleterious variation occurring at one or more sister sites. Here, I present data bearing on evolutionary theory that illustrates the manner in which any functional adaptation in duplicate genes is markedly constrained because of the compensatory utility provided by a sustained genetic redundancy. Specifically, a two-locus epistatic model of paralogous genes was simulated to investigate the degree of purifying selection imposed, and whether this would serve to impede any possible biochemical innovation. Three population sizes were considered to see if, as expected, there was a significant difference in any selection for robustness. Interestingly, physical linkage between tandem duplicates was actually found to increase the probability of any neofunctionalization and the efficacy of selection, contrary to what is expected in the case of singleton genes. The results indicate that an evolutionary trade-off often exists between any functional change under either positive or relaxed selection and the need to compensate for failures due to degenerative mutations, thereby guaranteeing the reliability of protein production.

In developmental and evolutionary biology, particular emphasis has been given to the relationship between transcription factors and the cognate cis-regulatory elements of their target genes. These constitute the gene regulatory networks that control expression and are assumed to causally determine the formation of structures and body plans. Comparative analysis has, however, established a broad sequence homology among species that nonetheless display quite different anatomies. Transgenic experiments have also confirmed that many developmentally important elements are, in fact, functionally interchangeable. Although dependent upon the appropriate degree of gene expression, the actual construction of specific structures appears not directly linked to the functions of gene products alone. Instead, the self-formation of complex patterns, due in large part to epigenetic and non-genetic determinants, remains a persisting theme in the study of ontogeny and regenerative medicine. Recent evidence indeed points to the existence of a self-organizing process, operating through a set of intrinsic rules and forces, which imposes coordination and a holistic order upon cells and tissue. This has been repeatedly demonstrated in experiments on regeneration as well as in the autonomous formation of structures in vitro. The process cannot be wholly attributed to the functional outcome of protein-protein interactions or to concentration gradients of diffusible chemicals. This phenomenon is examined here along with some of the methodological and theoretical approaches that are now used in understanding the causal basis for self-organization in development and its evolution.

All life depends on the biological information encoded in DNA with which to synthesize and regulate various peptide sequences required by an organism's cells. Hence, an evolutionary model accounting for the diversity of life needs to demonstrate how novel exonic regions that code for distinctly different functions can emerge. Natural selection tends to conserve the basic functionality, sequence, and size of genes and, although beneficial and adaptive changes are possible, these serve only to improve or adjust the existing type. However, gene duplication allows for a respite in selection and so can provide a molecular substrate for the development of biochemical innovation. Reference is made here to several well-known examples of gene duplication, and the major means of resulting evolutionary divergence, to examine the plausibility of this assumption. The totality of the evidence reveals that, although duplication can and does facilitate important adaptations by tinkering with existing compounds, molecular evolution is nonetheless constrained in each and every case. Therefore, although the process of gene duplication and subsequent random mutation has certainly contributed to the size and diversity of the genome, it is alone insufficient in explaining the origination of the highly complex information pertinent to the essential functioning of living organisms.

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The success of extant species is largely due to their ability to adapt in the face of constantly changing environmental conditions. Natural selection is the biological mechanism that takes advantage of opportunities to promote spontaneous variations and facilitate evolutionary development. The character of this biological opportunism is considered here, placing it firmly within the context of various social and economic principles-notably individualism, industrialism, utilitarianism and consequentialism-that have characterised the philosophy of the modern era. However, this purely opportunistic approach, and its myopic emphasis on immediate problem solving, has serious shortcomings within both life and business practice. These are examined here in contrast to some of the alternative approaches found in biology and economics theory. The nature and relationship of function to utility in biology is also given particular consideration, as is the issue of incrementalism in the development of complex adaptive features. The methodological reductionism at the heart of evolutionary biology certainly does offer insightful empirical results reported in the scientific literature. Nonetheless, natural selection is observed to be a purely reflexive mechanism and not one capable of producing the kind of innovation necessary for the more revolutionary changes in an organism's systems.