Turning chitin into chitosan: How AaCDA enzymes help Alternaria alternata hide from host defenses

A research team led by Professor Yongcai Li at Gansu Agricultural University has investigated the biological functions of the chitin deacetylases AaCDA1 and AaCDA2 in Alternaria alternata, the fungal pathogen responsible for pear black spot. The study, published in the journal Mycology, explores how these enzymes contribute to the pathogen's development and its interaction with host plants.

The researchers found that the deletion of either AaCDA1 or AaCDA2 did not result in significant changes to colony morphology, biomass, or conidiation. However, these genes play an important role in the differentiation of infection structures, as the deletion mutants exhibited reduced rates of appressorium formation and a decreased ability to penetrate the host epidermis compared to the wild-type strain. In cell wall stress assays, while the mutants maintained stability under various environmental pressures, they showed sensitivity to specific cell wall-disturbing agents, indicating that these enzymes are involved in maintaining the structural integrity of the fungal cell wall.

Furthermore, the study demonstrated that AaCDA1 and AaCDA2 participate in the enzymatic conversion of cell wall chitin into chitosan. This modification serves to reduce the visibility of the pathogen during the infection process. When these genes are absent, the increased exposure of chitin allows the host to detect the fungus more effectively. This recognition subsequently triggers a series of immune responses, including the accumulation of reactive oxygen species (ROS) and the upregulation of defense-related genes, which ultimately restricts the colonization and pathogenicity of the fungus on pear and other potential hosts. These findings suggest that these deacetylases regulate both fungal developmental adaptation and immune evasion during the infection process.