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product finally turns on gene A, which carries out an essential organismal function. Pathways involving only inhibitory steps also exist, and these lead to an alternating series of high and low expression, depending on the state of the first gene in the pathway. It is often unclear whether such complexity has any advantages over the simple constitutive expression or self-regulation of the final member of the pathway.

In principle, pathway augmentation may be driven entirely by the nonadaptive processes of duplication, degeneration, and genetic drift. Consider the series of regulatory states for gene A in Fig. 5.3. In the simplest case, A carries out some function in a self-sufficient fashion, but in a series of steps, it can become completely reliant on upstream activation by transcription factor B. A scenario like this could unfold in the following way. Initially, A becomes sensitive to activation by B, either because gene A has acquired a binding site for factor B, or because factor B acquires a fortuitous mutation that causes it to serve as an activator of A. At this point, gene A has redundant activation pathways, and is therefore insensitive to loss of one of them. Should a degenerative mutation cause a redundantly regulated allele of A to lose the ability to self-regulate, B will have been established as an essential activator, i.e., the pathway will have been augmented by a step. In principle, this process could be repeated anew as B acquires sensitivity to a further upstream gene C and loses the ability to constitutively express.

FIGURE 5.3 A series of allelic states for locus A, defined by the ability to self-express and/or be activated by an upstream transcription factor B. Mutational rates of gain and loss of regulatory abilities are denoted by ug and ul, here for simplicity assumed to be the same for both self-activation and upstream activation. The redundantly regulated allele is invulnerable to single-loss mutations.



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