Many organisms exhibit visually striking spotted or striped pigmentation patterns. Turing's reaction-diffusion model postulates that such periodic pigmentation patterns form when a local autocatalytic feedback loop and a long-range inhibitory feedback loop interact. At its simplest, this network only requires one self-activating activator that also activates a repressor, which inhibits the activator and diffuses to neighboring cells. However, the molecular activators and repressors fully fitting this versatile model remain elusive. Here, we characterize an R2R3-MYB activator and an R3-MYB repressor in monkeyflowers that correspond to Turing's model and explain how periodic anthocyanin spots form. Notably, disrupting this pattern impacts pollinator visitation. Thus, subtle changes in simple reaction-diffusion networks are likely essential contributors to the evolution of the remarkable diversity of periodic pigmentation patterns in flowers. MaintextPeriodic pigmentation patterns like the stripes of zebras, the spiral pigmentation of seashells, and the petal spots of many flowers have fascinated biologists and mathematicians for centuries. One proposed developmental explanation for how such periodic patterns form is Turing's reactiondiffusion model (1), in which dynamic and autonomous patterns are generated simply owing to the interaction of an activator and a repressor. The activator self-activates and activates the repressor, which then diffuses and inhibits the activator along the diffusion path. This mechanism amplifies initial cellular fluctuations into tissue-level spatial patterns (2-4). Computer simulations suggest that by tinkering with the diffusion constants and the kinetics of the activator-repressor interaction, this simple circuit can recapitulate the immense diversity of pigmentation patterns observed in nature (3). However, the molecular identities and dynamics of actual activator-repressor pairs that fulfill the classic Turing model for pigment patterning have remained elusive. Anthocyanin spots in flower petals provide an excellent empirical system to reveal the molecular basis for the formation and evolution of periodic pigmentation patterns. These patterns, which are highly diverse in the angiosperms even among different varieties of the same species (5,6), are known to serve as critical cues in plant-pollinator interactions (7-9); and the genetic network controlling anthocyanin pigment production is otherwise well described (10, 11).

While native populations are often adapted to historical biotic and abiotic conditions at their home site, populations from other locations in the range may be better adapted to current conditions due to changing climates or extreme conditions in a single year. We examine whether local populations of a widespread species maintain a relative advantage over distant populations that have evolved at sites better matching the current climate. Specifically, we grew lines derived from low-and high-elevation annual populations in California and Oregon of the common monkeyflower (Erythranthe guttata) and conducted phenotypic selection analyses in low-and high-elevation common gardens in Oregon to examine relative fitness and the traits mediating relative fitness. Californian low-elevation populations have the highest relative fitness at the low-elevation site, and Californian high-elevation populations have the highest relative fitness at the high-elevation site. Relative fitness differences are mediated by selection for properly timed transitions to flowering, with selection favoring more rapid growth rates at the low-elevation site and greater vegetative biomass prior to flowering at the high-elevation site. Fitness advantages for Californian plants occur despite incurring higher herbivory at both sites than the native Oregonian plants. Our findings suggest that a lag in adaptation causes maladaptation in extreme years that may be more prevalent in future climates, but local populations still have high growth rates and thus are not yet threatened.

Grass inflorescence development is diverse and complex and involves sophisticated but poorly understood interactions of genes regulating branch determinacy and leaf growth. Here, we use a combination of transcript profiling and genetic and phylogenetic analyses to investigate tasselsheath1 ( tsh1 ) and tsh4 , two maize genes that simultaneously suppress inflorescence leaf growth and promote branching. We identify a regulatory network of inflorescence leaf suppression that involves the phase change gene tsh4 upstream of tsh1 and the ligule identity gene liguleless2 ( lg2 ). We also find that a series of duplications in the tsh1 gene lineage facilitated its shift from boundary domain in nongrasses to suppressed inflorescence leaves of grasses. Collectively, these results suggest that the boundary domain genes tsh1 and lg2 were recruited to inflorescence leaves where they suppress growth and regulate a nonautonomous signaling center that promotes inflorescence branching, an important component of yield in cereal grasses.