Yanliu Wu, X Chen, Yuhao Du, Zhenhua Chen, Zhaoqian Yan, Runqian Peng, Kefu Yu
Corals are major biogenic sources of dimethyl sulfide (DMS), a climate-relevant gas derived from dimethylsulfoniopropionate (DMSP). However, the mechanisms regulating DMSP metabolism in corals under environmental stress remain largely unclear. As climate warming intensifies wildfires, the deposition of wildfire aerosols into coral reef regions has become a growing concern. Our study investigated the effects of wildfire fine particulate matter (PM 2.5 ) on DMSP metabolism and immune responses in Acropora formosa . PM 2.5 exposure significantly reduced the coral DMSP levels, impairing antioxidant defenses. The coral host upregulated both DMSP synthetic and catabolic genes, suggesting a compensatory response to oxidative stress, while Symbiodiniaceae showed limited transcriptional changes. Coral-associated bacterial communities exhibited reduced diversity and intensified antagonistic interactions, characterized by enrichment of DMSP-producing taxa and reduction of DMSP-degraders. Bacteria shifted toward the methylation pathway for DMSP synthesis, while DMSP catabolism favored the cleavage pathway under low stress and the demethylation pathway under high stress. However, these adaptive adjustments in DMSP metabolism were insufficient to compensate for DMSP depletion, leading to disruption of immune signaling, activation of apoptosis, and ultimately coral bleaching. Our study elucidates the mechanism by which wildfire aerosols disrupt coral sulfur metabolism, suppress coral-derived DMS emissions, and may potentially influence local climate regulation.