Abstract

Anthracnose of poplar caused byColletotrichum gloeosporioidesis a leaf disease that seriously affects poplar growth. The pathogen invades the host in the form of adherent cells, which generate turgor pressure through the metabolism of intracellular substances prior to penetrating the epidermis of poplar leaves. In this study, the expansion-related pressure of the mature appressorium of the wild-typeC. gloeosporioideswas approximately 13.02 ± 1.54 MPa at 12 h, whereas it was 7.34 ± 1.23 MPa and 9.34 ± 2.22 MPa in the melanin synthesis-related gene knockout mutants ΔCgCmr1and ΔCgPks1, respectively. TheCgCmr1andCgPks1genes were highly expressed at 12 h in the wild-type control, implying that the DHN melanin biosynthesis pathway may play an important role in the mature appressorium stage. The transcriptome sequencing analysis indicated that the upregulated melanin biosynthesis genes inC. gloeosporioides, such asCgScd1,CgAyg1,CgThr1,CgThr2, andCgLac1, are involved in specific KEGG pathways (i.e., fatty acid biosynthesis, fatty acid metabolism, and biotin metabolism). Therefore, we speculate that the melanin synthesis-related genes and fatty acid metabolism pathway genes contribute to the regulation of the turgor pressure in the matureC. gloeosporioidesappressorium, ultimately leading to the formation of infection pegs that enter plant tissues. These observations may reflect the co-evolution ofC. gloeosporioidesand its host.Keywords:Colletotrichum gloeosporioides;appressorium;turgor generation;DHN melanin biosynthesis