Yun Fang

The evolution of distinct lung architectures in birds (tubular air capillaries) and mammals (alveoli) represents a classic example of convergent evolution, yet their cellular differences remain poorly characterized. We present the comparative single-cell atlas of avian and mammalian lungs, revealing four key findings. First, we discover a persistent hybrid cell population (AT1/AT2) in neonatal and adult birds that disappears postnatally in mice, uncovering distinct strategies for lung maintenance. Second, cross-species comparisons highlight striking divergence in alveolar cell types, reflecting specialized adaptations to different respiratory demands. Third, avian lungs show unique molecular signatures in proliferation and saccular development pathways, potentially explaining their superior respiratory efficiency. Fourth, our viral receptor analysis uncovered differential ACE2 (SARS-CoV-2 receptor) expression but conserved EGFR (influenza A receptor), suggesting species-specific disease vulnerabilities. This work provides unprecedented insights into the evolutionary and developmental mechanisms shaping lung diversity in endotherms, with implications for respiratory biology, regenerative medicine, and zoonotic disease research.

Nest predation critically influences avian reproduction, with concealed nests typically assumed to be safer from nest predators. However, the expected positive relationship between nest concealment and survival has not been consistently observed across species. A hypothesis proposed by Skutch provides a possible explanation that parental care may increase nest predation risk by attracting predators. To test this hypothesis, we conducted a field experiment in the White‐bellied Redstarts (Luscinia phaenicuroides), which experience high predation rates despite highly concealed nests. Compared with active nests (with parental care), the same inactive nests after breeding had finished (without parental care) exhibited significantly higher daily survival rates and lower nest predation rates. Our findings support Skutch's hypothesis, and we presume that parental care provides cues for nest predators while the species' small body size limits nest defense. These findings provide insights into how parental behavior interacts with nest site selection to shape effective antipredator strategies.

High elevation imposes unrelenting and unavoidable hypoxia on species inhabiting these environments, providing an excellent natural setting for studying convergent or divergent evolution. By integrating measures of phenotypic variation, gene regulation, and functional performance, our study demonstrates that recent colonizers of high-elevation environments exhibit fundamentally different cardiovascular changes compared to long-term natives of these environments. Through the studying of heart morphological phenotypes, we showed that recent colonizers exhibit signs of cardiac hypertrophy, reflected by increased relative heart mass (heart mass/body mass) and cardiomyocyte size compared to their low-elevation relatives. In contrast, native species show no signs of cardiac hypertrophy and instead have 3-fold higher capillary densities than the colonizers, a change that likely enhances tissue oxygen diffusing capacity in the former. Using phylogenetic principal component analysis to quantify multivariate trait divergence, we show that native species are similar in cardiovascular phenotype and underlying gene expression, but differ appreciably from recent colonizers. We further demonstrate, using a functional assay, that differential expression of two genes (IRS2 and AKT1) in a conserved regulatory pathway mediates cardiomyocyte hypertrophy, which could explain the observed variation in cardiomyocyte size between native species and recent colonizers. This regulatory basis of variation in cardiac phenotype involves the differential expression of genes in a cardiomyocyte hypertrophy pathway that is conserved across birds, humans and other mammals. Collectively, our study highlights that evolutionary history is a critical determinant of cardiovascular variation in high-elevation environments.