Novel antifungal mechanism of oligochitosan by triggering apoptosis through a metacaspase-dependent mitochondrial pathway in Ceratocystis fimbriata

The antifungal effects of oligochitosan (OCS) against Ceratocystis fimbriata that causes black rot disease in sweet potato and its apoptosis mechanism were evaluated. OCS restrained the mycelial growth and spores germination of C. fimbriata, and decreased the ergosterol content of cell membrane. Transmission electron microscopy observation and flow cytometry analysis revealed that OCS induced morphology changes with smaller size and increased granularity of C. fimbriata, which was the typical feature of apoptosis. To clarify the apoptosis mechanism induced by OCS, a series of apoptosis-related parameters were analyzed. Results showed that OCS induced reactive oxygen species accumulation, Ca²⁺ homeostasis dysregulation, mitochondrial dysfunction and metacaspase activation, coupled with hallmarks of apoptosis including phosphatidylserine externalization, DNA fragmentation, and nuclear condensation. In summary, OCS triggered apoptosis through a metacaspase-dependent mitochondrial pathway in C. fimbriata. These findings have important implications for the application of OCS to control pathogens in food and agriculture.

Keywords: 2′,7′-Dichlorofluorescein diacetate (PubChem CID: 104913); 4',6-Diamidino-2-phenylindole (PubChem CID: 2954); Apoptosis; Chitosan; Oligochitosan; Oligochitosan (PubChem CID: 3086191); Phosphatidylserine (PubChem CID: 6323481); Propidium iodide (PubChem CID: 104981); Reactive oxygen species; mitochondrion.