Genetic analyses reveal wildfire particulates as environmental pollutants rather than nutrient sources for corals

Heterotrophic nutrients are crucial for coral growth and recovery from bleaching events. Although wildfire emissions are a potential source of these nutrients, their impact on corals was minimally investigated. In this microcosm experiment, Acropora formosa corals exhibited rapid tissue detachment upon exposure to wildfire fine particulate matter (PM 2.5 ). Physiological and genetic analyses revealed mechanisms associated with oxidation-reduction homeostasis and nutrient metabolism. Excessive hydrogen peroxide was generated as corals activated cytochrome P450 enzymes and the respiratory burst in phagocytic cells to metabolize PM 2.5, leading to oxidative damage, mitochondrial dysfunction, and cell apoptosis due to reduced superoxide dismutase activity and compromised glutathione antioxidant function. Subsequently, corals upregulated the transcriptions of genes which are related to tyrosine receptor proteins to regulate multicellular development for self-repair, increasing energy consumption. However, Symbiodiniaceae upregulated their metabolism and retained photosynthates, reducing nutrient supply to the coral host. Therefore, the host temporarily utilized lipid reserves via the glyoxylate cycle, but excessive consumption disrupted lipid and carbohydrate metabolism, ultimately weakening cell adhesion and causing coral tissue detachment. Additionally, the downregulation of HSP70 expression, potentially linked to decreased sacsin and mitochondrial apoptosis, accelerated coral heat bleaching. This study elucidates the mechanisms by which wildfire PM 2.5 at environmental concentrations poses risks to corals, particularly in a warming climate.