The light-induced mitochondrial heme-A synthase gene Bccox15 regulates spore longevity of Botrytis cinerea via affecting oxidative homeostasis

Conidia of plant pathogenic fungi represent specialized dormant cells that ensure long-term survival, dispersal, and infection. However, the mechanisms that sustain conidial dormancy and longevity remain poorly understood. Here, we identify the mitochondrial heme A synthase gene Bccox15 as a critical regulator of mitochondrial respiration, redox homeostasis, and long-term conidial viability in the necrotrophic pathogen Botrytis cinerea causing gray mold diseases on broad spectrum of plant crops. Specifically, the Bccox15 expression is induced by light and is highly enriched in aerial hyphae, conidiophores, and developing conidia. Deletion of Bccox15 does not completely deprive initial conidiation, but markedly reduces conidial viability after long-term resting, leading to progressive defects in germination and virulence potential of the aged conidia. Ultrastructural and cytological analyses reveal that Δ bccox15 undergo enhanced vacuolization, depletion of lipid droplets, and reduced trehalose accumulation in aged conidia. Moreover, Δ bccox15 displays attenuated heme biosynthesis in conidia. These changes are accompanied by mitochondrial hypertrophy, decreased mitochondrial membrane potential, and disrupted mitochondrial organization. At the colony level, loss of Bccox15 results in sustained respiratory activity, elevated colony temperature, and excessive reactive oxygen species accumulation in aged cultures. Collectively, our findings demonstrate that Bccox15 is associated with coordinating mitochondrial respiration and maintaining conidial dormancy and longevity.