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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.^[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.^[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.^[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. 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.

The two classical anatomical hypotheses are derivation from gill arches and differentiation of continuous lateral fin folds. Developmental co-option supplies an additional explanation for shared patterning mechanisms. The histories of the shoulder support, appendage blade and developmental programme need not be identical. Evaluating them separately allows evidence that initially appears contradictory to describe different components of the same evolutionary transition.

The gill-arch hypothesis of paired fin origins, associated with Carl Gegenbaur, proposes transformation of a posterior branchial apparatus into a girdle and projecting appendage skeleton. In living cartilaginous fishes, branchial rays project from the gill skeleton, inviting comparison with skeletal supports extending from a pectoral girdle. The historical archipterygium interpretation treated these as evidence for a gill-to-fin transformation. Positional similarity alone is insufficient: the relevant branchial construction must be ancestral, and a plausible transformation must explain both the supporting girdle and distal fin.

Developmental experiments provide stronger evidence for shared mechanisms than simple adult resemblance. Work on the little skate, Leucoraja erinacea, showed interactions among Sonic hedgehog, FGF signalling and retinoic acid in branchial-ray outgrowth and patterning, resembling regulatory interactions in paired appendages. The crucial inference is reuse of a spatial patterning system; expression of the same molecule by itself would be weaker evidence. Functional perturbation helps distinguish an active requirement from a coincidental expression domain.^[ref]

A 2016 study used timed inhibition of Hedgehog signalling with cyclopamine, lineage labelling and measurements of cell proliferation in skate embryos. Earlier inhibition disrupted branchial-ray polarity, while later inhibition reduced their production or expansion. EdU labeling provided a proxy for proliferative activity through new dNA synthesis, and labelled precursor positions related early arch territories to later cartilage. Solvent-treated controls are necessary because handling and drug vehicle can alter development; stage matching and general growth measurements are needed to distinguish pattern-specific effects from generalized retardation. These results support parallel roles for the signal in axial organization and progenitor expansion. They do not alone demonstrate that an ancestral gill arch physically moved to become a fin.^[ref]

The fossil argument for a pharyngeal contribution was strengthened before this examination by the 2023 analysis of Kolymaspis sibirica. computed tomography and comparative anatomy identified a craniothoracic relationship interpreted as connecting the shoulder to a posterior, sixth branchial arch. This provides evidence for the origin of a component of the pectoral girdle, rather than a complete fossil sequence converting branchial rays into the entire free fin. Homology of the articulation and the reconstruction of the head–trunk boundary remain important assumptions. A pharyngeal contribution to the girdle does not require a wholly pharyngeal origin for every appendicular tissue.^[ref]

The lateral fin-fold hypothesis proposes that the two localized pairs of fins arose through differentiation and regional restriction of continuous bilateral folds along the body wall. It predicts possible precursors extending through intervening pectoral and pelvic regions, with increased regional differentiation and locomotor control later. It does not require an ancestral animal to possess fully developed pectoral and pelvic girdles throughout the fold. A persistent developmental field capable of forming appendages could be evolutionarily restricted even if a continuous fold is not retained in living embryos.

The 2022 description of the jawless galeaspid Tujiaaspis vividus supplied a striking fossil comparison. Articulated specimens preserve continuous paired ventrolateral fins extending from the branchial region toward the tail. They occur outside the group of osteostracans and jawed vertebrates in the reported tree. Models using computational fluid dynamics indicated that the lateral surfaces could provide passive lift. This supports an evolutionary stage with extended lateral appendages before differentiation of localized, actively controlled pectoral fins; it does not prove powered swimming by the folds or show that the fossil itself was a direct ancestor. Surface reconstruction, swimming conditions and the assumed body geometry constrain the functional model.^[ref]

Other jawless stem relatives sharpen the proposed sequence. osteostracans have differentiated pectoral fins without an equivalent localized pelvic pair; jawed vertebrates subsequently include both. This distribution argues against assuming simultaneous origin of the two appendage pairs. In a fin-fold interpretation, anterior differentiation can precede restriction of the remaining competent body-wall region to a pelvic position. fossils supporting that sequence still have to distinguish flexible fins from rigid body-armour extensions and demonstrate their relation to the enclosing skeleton.

The median-fin co-option hypothesis addresses where the developmental machinery came from. median fins are evolutionarily older than the paired appendages. Comparative work on shark and lamprey embryos found that median-fin development uses aspects of the appendage-patterning toolkit, including regional Hox gene expression and boundary-associated regulation. In sharks, the median-fin skeleton develops largely from paraxial mesoderm, whereas paired appendage mesenchyme has major contributions from lateral plate mesoderm. Similar patterning despite different tissue sources supports redeployment of an older regulatory programme. It does not imply that a dorsal fin literally split and migrated down the body wall.^[ref]

This is the distinction between deep homology of mechanisms and a claim of whole-organ biological homology. Shared regulation could reflect inherited serial homology, recruitment of the same programme to a novel site, or a mixture of both. Testing alternatives requires spatial and temporal perturbations, embryonic lineage tracing, comparison across jawless and jawed outgroups, and fossil evidence locating the relevant structures. Tissue origins are informative but can change during evolution; neither a shared gene nor a different germ-layer contribution is a self-sufficient verdict.

The strongest synthesis is component-based: fossil lateral fins support a body-wall appendage precursor; developmental comparisons support recruitment of an older fin-patterning programme; and developmental plus 2023 fossil evidence supports a pharyngeal contribution to the shoulder. The remaining problem is to establish how those components were assembled and when regional pectoral and pelvic control evolved. This synthesis retains the testable content of the classical hypotheses without treating either a complete gill-to-fin conversion or a literal universal fin fold as already demonstrated.