= Solution
\b[<evolutionary developmental biology> explains many novelties as new uses, arrangements or regulation of inherited components.] A new organ need not require an entirely new set of <genes>: changes to a <gene regulatory network> can deploy existing activities at a new place, time or strength during <biological development>. Novelty in the resulting <phenotype> is therefore compatible with continuity of the underlying materials.
One route is <gene co-option>. A regulator already controlling a useful cellular program can acquire a new domain of <gene expression>, bringing downstream activities into a different structure. The important unit may be an entire interacting module, rather than a single <gene>. In the classic ectopic-eye experiment, targeted <gene expression> of <eyeless> in developing fruit-fly tissues induced eye structures in abnormal locations. This shows that competent tissues can deploy an existing developmental program when a regulatory input changes; it does not show that a regulator alone constructs an eye independently of its cellular context.<Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila by Georg Halder and others>[Science 267, pp. 1788–1792; targeted expression and differentiated ectopic eye structures]{ref} Shared regulators can constitute <deep homology> even where the final structures have different architectures. Sharing one regulator, however, is not sufficient to establish that two complete organs are homologous.
<cis-regulatory evolution> supplies a way to change one deployment while preserving others. A <transcription factor> may function in several tissues, giving coding changes extensive <pleiotropy>. A tissue-specific <enhancer> can instead change the spatial pattern of <gene expression>. In sticklebacks, recurrent deletion of a pelvic <enhancer> of <Pitx1> contributes to pelvic reduction while leaving other deployments of the <gene> available. Mapping, <enhancer> assays and transgenic restoration connected the regulatory region to the skeletal outcome.<Adaptive evolution of pelvic reduction in sticklebacks by recurrent deletion of a Pitx1 enhancer by Yingguang Frank Chan and others>[Science 327, pp. 302–305; pelvic enhancer deletions, reporter activity and transgenic rescue]{ref} This is primarily a reduction of a structure, but it demonstrates the regulatory modularity that can also enable gains or transformations. Not every <enhancer> is tissue-specific, and regulatory changes can themselves have extensive <pleiotropy>.
Developmental transformations can also involve <heterochrony>, a change in timing or duration, and <heterotopy>, a change in location. Extending a growth phase can alter a structure's proportions; moving a signaling source can alter a pattern. Changes in <Hox genes> or their regulation can alter regional identities along the body axis, while changes in downstream targets can modify one segment without changing every segment. <serial homology> supplies repeated structures that can subsequently specialize. These routes modify inherited developmental processes, but the resulting functional organization can still be new. The size of an adult change is not a reliable measure of the number of underlying <mutations>.
<gene duplication> makes another form of reuse possible. Initially the copies may share a function. <subfunctionalization> can partition ancestral deployments between them; <neofunctionalization> can give one copy a new function while the other preserves an old one. Changes in regulatory connections and <protein> sequence can then accumulate with fewer immediate costs. Duplication is not guaranteed to generate novelty: most extra copies may be lost or change <gene dosage>, and retaining a copy requires an account of its inheritance and effects on <genotype fitness>. Similarly, <exaptation> describes recruitment of an existing character to a new use; it is a functional historical claim, whereas <gene co-option> names a developmental mechanism that may underlie that history.
Reuse can also generate a new biochemical function. Comparative sequence analysis traced Antarctic fish <antifreeze glycoproteins> to an ancestral <trypsinogen> <gene>: retained ancestral segments and amplification of a short sequence helped construct a new repetitive coding region.<Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish by Liangbiao Chen and others>[PNAS 94, pp. 3811–3816; comparison of gene structures and reconstruction of the amplification process]{ref} An inherited coding framework supplied material for an ice-binding protective product with a different function. This is a molecular novelty rather than a new organ, but it illustrates how reuse can build a new activity rather than merely preserve or remove an old one.
Development also changes which variants are accessible. A <gene regulatory network> can buffer many perturbations but respond sharply to a particular change, so <mutation> does not sample all imaginable forms equally. <developmental bias> can make similar outcomes recur in independent lineages. <natural selection> then filters the variants that actually arise; developmental accessibility and selective advantage are distinct explanations that can operate together. Repeated involvement of the same <gene> might reflect its useful regulatory position, an unusually high local <mutation rate>, or inheritance of the same ancestral <allele>. Distinguishing these requires comparative and functional evidence.
The quotation should not be interpreted as denying new sequence or new function. <de novo gene birth> can produce a newly translated product from previously <non-coding DNA>; <mutations> can create a new regulatory binding site; and a genuinely new interaction can arise between old components. Such cases challenge the narrower assertion that every new <gene> is a modified pre-existing coding <gene>. They still involve changes to existing <DNA>, cellular machinery and developmental context, rather than construction without material antecedents. Failure to detect a distant sequence relative is also insufficient evidence for <de novo gene birth>, because rapid divergence and incomplete sampling can hide ancestry.
A convincing evolutionary developmental account therefore combines a <phylogenetic tree> establishing ancestral states, comparative measurements at matched developmental stages, and perturbations that connect the proposed change to the new outcome. For a candidate <enhancer>, compare ancestral and derived sequences in the same integration context, include an inactive construct and the normal sequence as controls, and test replacement or rescue at the endogenous <genetic locus>. A reporter alone tests regulatory potential, not the necessity of the sequence in its native context. \b[Novelties commonly arise by modifying inherited developmental systems, but their new organization and function are real, and the origin of new genes cannot be reduced to duplication alone.]
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