Figure 5.

A simplified schematic diagram of the infection mechanism of Penicillium digitatum on citrus. After P. digitatum colonization in citrus wounds, it up-regulated the expression of the iron transporter protein for Fe absorption from the citrus wounds to meet its requirements for growth. Among them, the up-regulation of Fe²⁺ and ethylene-forming enzyme (EFE) in P. digitatum promoted ethylene synthesis. Ethylene is a growth and development promoter in P. digitatum. Again, genes that synthesize extracellular plant cell wall degrading enzymes and organic acid were upregulated by P. digitatum to promote degradation of plant cell walls into glucose and other carbon sources, providing nutrients necessary for growth. This process kills citrus cells and makes wound tissues rot. However, Cell wall degrading enzymes (CWDEs) and ethylene also activated PAMP-triggered immunity (PTI) of citrus to inhibit the infection of P. digitatum, which results in a series of oxidative bursts in citrus wounds. In order to resist oxidative stress, the expression of anti-oxidant related components such as catalase was up-regulated by P. digitatum. It is noteworthy that P. digitatum also secreted some effectors like LysM domain proteins and ecosis-inducing protein that inhibits the PTI of citrus.