Developmentally cascading structures do not lose evolutionary potential, but compound developmental instability in rat molars.

Increasing variability down serially segmented structures, such as mammalian molar teeth and vertebrate limb segments, is a much-replicated pattern. The same phenotypic pattern has conflicting interpretations at different evolutionary scales. Macroevolutionary patterns are thought to reflect greater evolutionary potential in later-forming segments, but microevolutionary patterns are thought to reflect less evolutionary potential and greater phenotypic plasticity. We address this conflict by recalculating evolutionary potential (evolvability) from a systematic review of published mammalian molar sizes, then directly measure phenotypic plasticity from a controlled feeding experiment. Effects on lengths and widths are discordant in a way that suggests general growth pathways have a role in phenotypically plastic dental responses to nutrition. Effects on successive trait means do not necessarily increase downstream, contrary to long-standing hypotheses. We confirm prior findings of increasing non-inherited variance downstream, showing decoupling between effects on trait mean and variance. These patterns can be explained by a cascading model of tooth development compounding the effect of developmental instability as an influence separate from general environmental effects on the developing embryo. When evaluated in terms of evolvability, later-developing molars are equally or more evolvable than earlier-developing molars, aligning their microevolutionary potential with macroevolutionary patterns in other serially segmented structures.