This randomized trial examines gene expression in salamanders infected with Bsal, suggesting ways to mitigate biodiversity loss.
Changes in gene expression during host–pathogen interactions reveal species' functional responses and provide insight into the mechanisms by which pathogens impact biodiversity. The pathogen Batrachochytrium salamandrivorans (Bsal) poses a major threat to salamander diversity, particularly in global biodiversity hotspots. In the most species‐rich salamander family, Plethodontidae, infection outcomes vary markedly, suggesting that hosts play a role in mediating susceptibility. Despite this variation, salamander defence mechanisms against Bsal, as well as the pathogen's capacity to facilitate multi‐host infection, remain largely unexplored. Here, I characterised gene expression changes associated with salamander–Bsal interactions using a multispecies comparative framework that integrated host and pathogen functional mechanisms. I identified variation in host responses alongside a conserved expression pattern among plethodontid salamanders, and uncovered Bsal's capacity to adjust its genetic machinery in relation to host susceptibility and, potentially, co‐infection with its sister taxon, Batrachochytrium dendrobatidis (Bd). These findings provide insight into the biological mechanisms underlying salamander–Bsal interactions, highlighting a pathway involved in Bsal virulence mediated by calmodulin. This study underscores the need to characterise gene expression changes in both host and pathogen simultaneously to better understand species interactions, and proposes that these changes should be modelled within the parasite–mutualist continuum. Comparative frameworks incorporating multiple host species are also essential for characterising conserved responses to infection, and ultimately for anticipating, preventing and mitigating the potential negative impacts of Bsal on salamander biodiversity.
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María Torres‐Sánchez (2026) studied this question.
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