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Abstract The genomic characteristics of adaptively radiated groups could contribute to their high species number and ecological disparity, by increasing their evolutionary potential. Here, we explored the genomic variation of Anolis lizards, focusing on three species with distinct phenotypes: A. auratus, one of the species with the longest tail; A. frenatus, one of the largest species; and A. carolinensis, one of the species that inhabits the coldest environments. We assembled and annotated two new chromosome-level reference genomes for A. auratus and A. frenatus, and compared them with the available genomes of A. carolinensis and A. sagrei. We evaluated the presence of structural rearrangements, quantified the density of repeat elements, and identified potential signatures of positive selection in coding and regulatory regions. We detected substantial rearrangements in scaffolds 1, 2 and 3 of A. frenatus different from the other species, in which the rearrangement breakpoints corresponded to hotspots of developmental genes. Further, we detected an accumulation of repeats around key developmental genes in anoles and phrynosomatid outgroups. Finally, coding sequences and regulatory regions of genes relevant to development and physiology showed variation that could be associated with the unique phenotypes of the analyzed species. Our results show examples of the hierarchical genomic variation within anoles, that could provide the substrate that promoted phenotypic disparity and contributed to their adaptive radiation. 

Abstract Sexual size dimorphism is common throughout the animal kingdom, but its evolution and development remain difficult to explain given most of the genome is shared between males and females. Sex-biased regulation of genes via sex hormone signaling offers an intuitive mechanism by which males and females could develop different body sizes. One prediction of this hypothesis is that the magnitude of sexual size dimorphism scales with the number of androgen response elements or estrogen response elements, the DNA motifs to which sex hormone receptors bind. Here, we test this hypothesis using 268 mammalian species with full genome assemblies and annotations. We find that in the two smallest-bodied lineages (Chiroptera and Rodentia), sexual size dimorphism increases (male-larger) as the number of androgen response elements in a genome increases. In fact, myomorph rodents—which are especially small-bodied with high sexual size dimorphism—show an explosion of androgen receptor elements in their genomes. In contrast, the three large-bodied lineages (orders Carnivora, Cetartiodactyla, and Primates) do not show this relationship, instead following Rensch's Rule, or the observation that sexual size dimorphism increases with overall body size. One hypothesis to unify these observations is that small-bodied organisms like bats and rodents tend to reach peak reproductive fitness quickly and are more reliant on hormonal signaling to achieve sexual size dimorphism over relatively short time periods. Our study uncovers a previously unappreciated relationship between sexual size dimorphism, body size, and hormone signaling that likely varies in ways related to life history.