TrcrtB regulates carotenoid biosynthesis, stress tolerance, conidiation and pathogenicity in the postharvest pink rot fungus, Trichothecium roseum.

Abstract

Trichothecium roseum is a highly destructive postharvest pathogenic fungus that causes pink mold rot in various fruit and leads to significant agricultural and economic losses. Phytoene is crucial for phytopathogens, but the molecular mechanism by which the phytoene synthase gene crtB regulates fungal pathogenicity remains largely unclear. In this study, we evaluated the functions of TrcrtB a phytoene synthase, in T. roseum via in vivo and in vitro assays. Our results showed that knock-out of TrcrtB showed inhibition of production of phytoene and its relevant downstream metabolites, such as lycopene, carotenes and carotenal, resulting in colorless colony and branching at the mycelial edges in the knockout mutant ΔTrcrtB. Compared with the wild type (WT) strain, the colony expansion was significantly reduced 35% at 5 days post-inoculation (dpi), and conidiation was notably decreased to 45%, 36%, and 70% at 3, 5, and 7 dpi in ΔTrcrtB in vitro. Scanning electron microscope observation revealed similar results. Moreover, the ΔTrcrtB showed higher sensitivity to abiotic stresses than WT, as evidenced by inhibition rates of ΔTrcrtB colony expansion up to 71.76% (menadione), 47.73% (Congo red), 23.01% (SDS), and 17.13% (KCl). The pathogenicity of ΔTrcrtB was dramatically impaired by decreasing the rotten area up to 85.26% on apple fruit and 70.30% on pears fruit. These results suggest that TrcrtB and phytoene are critical for development, stress tolerance and pathogenicity of T. roseum. Collectively, our study highlights the roles of TrcrtB and phytoene in the pathogenic fungus T. roseum, providing new insights into the molecular mechanisms of pink rot pathogenesis.