The CgATG16 Was Involved in Growth, Development and Virulence Through Autophagy Modulation in the Rubber Tree...

Colletotrichum gloeosporioides causes rubber tree anthracnose and leads to serious loss in natural rubber production. Autophagy is a highly conserved process to maintain nutrient recycling and plays important roles in growth, development and pathogenicity in plant pathogenic fungi. The process of autophagy is modulated by a series of autophagy-related (ATG) genes. ATG16 is a subunit of the ATG12-ATG5-ATG16 complex which functions in a manner analogous to an E3-like enzyme which is essential for autophagosome formation. However, the function of the ATG16 homolog in C. gloeosporioides remains unknown. In this study, the ATG16 homolog of C. gloeosporioides was identified and named as CgATG16. The expression level of CgATG16 was particularly higher in conidium, germination, appressorium, and the early stage of infection, and significantly induced by nutritional deficiency. Absence of CgATG16 led to slower colony growth, decreased conidia production and germination rate, longer germ tube cells, lower appressorium formation rate and impaired pathogenicity to rubber tree leaves. Absence of CgATG16 resulted in lower melanin content with decreased expression of polyketide synthase gene CgPKS1 and scytalone dehydratase gene CgSCD1. Moreover, absence of CgATG16 also led to the universal autophagy marker ATG8-GFP failing to enter into the vacuoles in mycelium and during appressorium development with a significantly reduced autophagosome number. Both rapamycin and cyclic adenosine monophosphate (cAMP) partially restored the appressorium formation ability in CgATG16 knockout mutant. Absence of CgATG16 increased the activity of target of rapamycin (TOR) kinase and decreased the content of cAMP. These data suggest that CgATG16 contributes to the pathogenicity of C. gloeosporioides to the rubber tree by regulating the mycelium growth, melanin synthesis and the formation of invasion structure, and this process is related to autophagy mediated by TOR and cAMP signaling.