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FIGURE 5.2 The passive emergence of specialized gene functions via nonadaptive processes of duplication, degenerative mutation, and random genetic drift. (Left) Regulatory elements (transcription-factor binding sites) are depicted on the left, with each regulatory element coded according to the transcription factor that binds to it. (Right) Allele-specific utilizations of transcription factors are depicted. Transcription factors denoted by black and white are ubiquitously expressed, whereas those denoted by hatching and crosshatching are each expressed in single, non-overlapping tissues. For this particular gene, within their respective tissues, the hatched and crosshatched transcription factors are redundant with respect to the white factor, but the additional black factors are essential for complete expression. Three hypothetical phases of gene architectural modification are shown. (Top) Accretion and degeneration of transcription-factor binding sites. The initial allele (a) is expressed in an identical manner in both tissues, but the regulatory region sequentially acquires the hatched and crosshatched elements. The redundant white element is then vulnerable to loss by degenerative mutation, yielding a descendant allele with a semi-independent mode of expression, as the black element is still essential to expression in both tissues. At this stage all four alleles (a–d) are interchangeable, as each of them achieves the same pattern of phenotypic expression. (Middle) Regulatory-region duplication, degeneration, and complementation. The entire enhancer region is tandemly duplicated, with each component then losing a complementary (hatched/crosshatched) element. The resultant allele has become modularized in the sense that it harbors two independently mutable subfunctions denoted by the hatched and crosshatched open boxes; a mutation in either region has effects confined to a single tissue. (Bottom) Gene duplication and subfunctionalization by degenerative mutation. The entire gene is duplicated, with each copy becoming silenced by degenerative mutation for a complementary subfunction. The expression of each copy is now confined to a single tissue.

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