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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. 

Abstract In mammals, a temporary endocrine gland called the corpus luteum forms on the ovary shortly after ovulation and is required for the initiation and maintenance of early pregnancy. However, the corpus luteum persists even when fertilization or pregnancy does not occur, and species-specific variation in the length of this persistence remains enigmatic. Here we perform a comparative evolutionary study across 72 species and show that corpus luteum lifespan in nonpregnant females is positively correlated with gestation length. We argue that the most likely explanation for this correlation is physiological inertia. The corpus luteum begins secreting progesterone prior to implantation, and when pregnancy does not occur it takes time for females to degrade it and prepare the next reproductive cycle. Our study suggests that this physiological inertia is stronger in species with long gestation times. 

Abstract A fundamental goal in evolutionary biology and population genetics is to understand how selection shapes the fate of new mutations. Here, we test the null hypothesis that insertion–deletion (indel) events in protein-coding regions occur randomly with respect to secondary structures. We identified indels across 11,444 sequence alignments in mouse, rat, human, chimp, and dog genomes and then quantified their overlap with four different types of secondary structure—alpha helices, beta strands, protein bends, and protein turns—predicted by deep-learning methods of AlphaFold2. Indels overlapped secondary structures 54% as much as expected and were especially underrepresented over beta strands, which tend to form internal, stable regions of proteins. In contrast, indels were enriched by 155% over regions without any predicted secondary structures. These skews were stronger in the rodent lineages compared to the primate lineages, consistent with population genetic theory predicting that natural selection will be more efficient in species with larger effective population sizes. Nonsynonymous substitutions were also less common in regions of protein secondary structure, although not as strongly reduced as in indels. In a complementary analysis of thousands of human genomes, we showed that indels overlapping secondary structure segregated at significantly lower frequency than indels outside of secondary structure. Taken together, our study shows that indels are selected against if they overlap secondary structure, presumably because they disrupt the tertiary structure and function of a protein. 

The baculum, a bone in the penis of many mammal species, shows an astonishing level of morphological divergence between species. Despite hundreds of years of interest, biologists have been unable to directly test its function. The goal of the current study is to uncover molecular details that could allow selective disruption of the baculum while allowing normal sexual differentiation and skeletal development. We compare patterns of androgen receptor binding and single cell gene expression in the developing penis, forelimbs and hindlimbs of mice. We identified chondrocytes in all three tissue types, but those from the developing penis show several unique features, including a population of chondrocytes that express bothRunt-related transcription factor 2(Runx2) andAndrogen receptor(Ar). By combining aRunx2-Cre allele with a floxedArallele in mice, we selectively knocked out androgen signaling in late chondrocytes, resulting in a range of defects in baculum morphology. Males with the most disrupted bacula were unable to copulate, and their bacula appears to be disconnected from the corpus cavernosum muscle. Our study provides insights into the diversity of molecular mechanisms leading to bone and offers the first opportunity to directly test the function of the baculum.