CgHog1 controls the adaptation to both sorbitol and fludioxonil in Colletotrichum gloeosporioides.

The HOG (high-osmolarity glycerol) pathway is critical for the appropriate adaptation to adverse conditions. Here, we demonstrated that the deletion of CgHog1 resulted in enhanced sensitivity to osmotic stress and increased resistance to fludioxonil in the poplar anthracnose fungus Colletotrichum gloeosporioides. The accumulation of chitin around hyphal tips was obviously decreased in the ΔCgHog1 strain under sorbitol, whereas it strongly was increased in the response to fludioxonil compared with the wild type. To investigate the underlying mechanism of CgHog1-mediated adaption to osmotic stress and fludioxonil, transcriptomic profiles were performed in both the ΔCgHog1 strain and the wild type under the treatment of sorbitol and fludioxonil, respectively. Under sorbitol, genes associated with glycolysis, lipid metabolism, and accumulation of soluble sugars and amino acids were differentially expressed; under fludioxonil, vesicle trafficking-related genes were highly downregulated in the ΔCgHog1 strain, which was consistent with abnormal vacuoles distribution and morphology of hyphae, indicating that the growth defect caused by fludioxonil may be associated with disruption of endocytosis. Taken together, we elucidated the adaptation mechanisms of how CgHog1 regulates appropriate response to sorbitol and fludioxonil via different metabolism pathways. These findings extend our insights into the HOG pathway in fungi.

The Mitogen-Activated Protein Kinase CgMK1 Governs Appressorium Formation, Melanin Synthesis, and Plant Infection of Colletotrichum gloeosporioides.

The fungus Colletotrichum gloeosporiodes infects plant hosts with a specialized cell called an appressorium, which is melanized and required for plant cell wall penetration. Here, we show that the mitogen-activated protein kinase CgMK1 governs appressorium formation and virulence in the poplar anthracnose fungus C. gloeosporioides. Deletion of CgMK1 impairs aerial hyphal growth and biomass accumulation, and CgMK1 is responsible for the expression of melanin biosynthesis-associated genes. CgMK1 deletion mutants are unable to form appressorium and lose the capacity to colonize either wounded or unwounded poplar leaves, leading to loss of virulence. We demonstrate that the exogenous application of cAMP fails to restore defective appressorium formation in the CgMK1 deletion mutants, suggesting that CgMK1 may function downstream or independent of a cAMP-dependent signal for appressorium formation. Moreover, CgMK1 mutants were sensitive to high osmosis, indicating that CgMK1 plays an important role in stress response. We conclude that CgMK1 plays a vital role in regulating appressorium formation, melanin biosynthesis, and virulence in C. gloeosporiodes.