= Solution
\b[Knowing the molecular basis of a behaviour is not a prerequisite for understanding its <evolution> or many of its evolutionary consequences. Evidence about transmission is essential for claims of inherited change, while detailed <genetic architecture> becomes essential for particular mechanistic predictions.] The claim therefore depends on what is meant by a genetic basis and on the explanatory question being asked.
<Tinbergen's four questions> distinguish mechanism, development, adaptive significance and evolutionary history. Identifying a neural or molecular mechanism helps explain how a response is produced; it does not automatically show why a variant spread, whether it currently increases <reproductive success>, or whether the same mechanism generated the ancestral transition. Conversely, a well-supported evolutionary explanation can begin with experimentally demonstrated <biological fitness> consequences and transmission without a complete molecular account. These explanatory levels are complementary rather than substitutes. <On aims and methods of Ethology by Nikolaas Tinbergen>[Zeitschrift für Tierpsychologie 20, pp. 410–433; causation, development, survival value and evolution]{ref}
The phrase genetic basis can refer to several different achievements: identifying inherited variation; estimating the number and effects of contributing <genetic loci>; finding a causal nucleotide change; or describing every <gene> required for development of the relevant sensory and motor systems. These are not equivalent. Many <genes> can be necessary for an animal to perform an action while none explains variation in that action within the studied population. Knocking out a broadly required neural <gene> and eliminating courtship does not identify an evolutionary substitution for a naturally varying <mate preference>.
<quantitative genetics> can predict a response without naming the causal molecular variants. Under the appropriate additive, generational and environmental assumptions, the <multivariate breeder's equation> gives:
$$
\Delta\overline{\mathbf z}=\mathbf G\boldsymbol\beta,
$$
where $\mathbf G$ is the <additive genetic covariance matrix> and $\boldsymbol\beta$ the vector of <phenotypic selection gradients>. Behavioural measurements, <pedigrees>, repeated observations and <reproductive success> can therefore estimate whether and in what direction a response is expected. The covariances matter: selection favouring exploration can produce a correlated response in aggression or constrain the response when their <biological fitness> effects conflict. Naming an exploration-related <gene> would not replace this population-level information.
These estimates require strong controls. <behavioural repeatability> is consistency among observations of the same individual; it can reflect persistent environment as well as inherited differences and is not equivalent to <heritability>. Parent–offspring resemblance can also reflect teaching, maternal provisioning or shared habitat. <cross-fostering>, <common garden experiments> and appropriately structured breeding designs help separate these alternatives. <heritability> is conditional on the sampled population and environment, not a measure of immutability. A response measured in one environment may fail elsewhere because of <genotype-environment interaction> or altered selection. Thus ignorance of exact molecular variants is compatible with informative prediction, but ignorance of transmission and its confounders is not.
Molecular work adds power when it establishes a causal link to naturally occurring variation. In <Drosophila melanogaster>, rover and sitter food-search variants were connected to the <foraging gene>, which encodes a <cGMP-dependent protein kinase>. Mapping, enzyme activity and transgenic rescue linked the molecular difference to behavioural performance; comparable locomotion without food helped exclude a general activity explanation. <Natural Behavior Polymorphism Due to a cGMP-Dependent Protein Kinase of Drosophila by K. A. Osborne and others>[Science 277, pp. 834–836, Tables 1–3; foraging variants, kinase activity and transgenic rescue]{ref} This is much stronger than finding a statistical association between a <gene> and a behavioural score. Nevertheless, the experiment alone does not establish which ecological conditions historically maintained the polymorphism. That requires <biological fitness> comparisons across resources, densities and frequencies, with genetic-background controls.
<genetic architecture> is particularly informative when <animal behaviour> changes <gene flow>. In <Heliconius melpomene> and <Heliconius cydno>, mapping identified several major regions associated with male mating preferences; one lay close to the wing-pattern regulator <Optix>. Tight <genetic linkage> can help maintain associations between a mating cue and preference despite exchange between lineages. It does not establish <pleiotropy>, and courtship assays must distinguish attraction from the female's response and subsequent mating. <Genetic dissection of assortative mating behavior by Richard M. Merrill and others>[PLoS Biology 17, e2005902; preference QTLs, linkage to optix, and limitations of courtship assays]{ref} Here molecular localization helps evaluate whether a proposed route to <reproductive isolation> is genetically feasible. A preference could still have been shown to reduce heterospecific mating before its contributing regions were mapped.
The influence of one individual's <animal behaviour> on another's development further complicates a simple own-genotype explanation. Maternal provisioning in <Onthophagus taurus> was studied using a breeding design that separated direct and maternal genetic contributions to offspring traits. <The genetics of maternal care: direct and indirect genetic effects on phenotype in the dung beetle Onthophagus taurus by John Hunt and others>[PNAS 99, pp. 6828–6832; paternal half-sib design, brood mass and maternal contributions]{ref} An <indirect genetic effect> occurs when another individual's inherited properties alter the focal individual's <phenotype>. Such effects change the environment in which selection acts and can alter expected evolutionary responses. Identifying only the offspring's molecular variants would miss an important part of the causal system. Conversely, an observed maternal effect is not automatically a maternal genetic effect; provisioning can vary for environmental reasons.
Transmission need not follow genetic parentage. In wild <great tits>, experimenters trained demonstrators to use alternative puzzle-box techniques and followed the spread of the introduced variants. Persistent local traditions and preferential adoption of the common local technique supported <social learning> and conformist transmission. <Experimentally induced innovations lead to persistent culture via conformity in wild birds by Lucy M. Aplin and others>[Nature 518, pp. 538–541; seeded puzzle-box techniques and social diffusion in wild great tits]{ref} The experiment established a route of behavioural inheritance without identifying a molecular difference between the techniques' users. It did not prove that <learning> ability has no inherited basis, or that the new tradition changed <allele frequencies>. Rather, it shows why an account of behavioural change needs to identify the relevant transmission process instead of assuming it.
Even a learned response with no demonstrated inherited differences can influence subsequent <evolution>. A new resource use can alter selection on digestion; a socially learned mating signal can alter <assortative mating>; habitat choice can change contact with other populations. The immediate causal effect can be tested by manipulating the action or its social transmission and measuring <biological fitness> or exchange. To claim ensuing genetic <adaptation>, one must additionally show inherited change. To explain exactly which variants can respond, how quickly, and with what correlated effects, information about <genetic architecture> becomes increasingly valuable.
The most productive programme therefore combines behavioural intervention, transmission studies, <biological fitness> measurement and molecular analysis when it addresses an unresolved mechanism. Candidate variants should be tested across natural genetic backgrounds and environments, preferably with targeted perturbation and rescue; historical claims also need comparative or temporal evidence. \b[Exact molecular knowledge is neither sufficient nor universally necessary: the necessary evidence is the evidence that connects the particular behavioural difference, its transmission and its measured evolutionary consequence.]
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