| MAPK(mitogen-activated protein)is a highly conserved protein kinase in eukaryotes,which performs biological functions through phosphorylation of target molecules.The HOG(high-osmolarity glycerol)pathway is critical for the appropriate adaptation to adverse conditions,such as osmotic,oxidative,heat,low PH and fungicidal stresses.Colletotrichum gloeosporioides is one of the main pathogens of poplar anthracnose.In order to analyze the mechanism of Cg Hog1 in regulating fungal growth and development,pathogenicity,and stress adaptation,genetic and functional genomics methods were used to elaborate the molecular mechanism of Cg Hog1 in response to high osmotic pressure and fludioxonil.The main results are as follows: 1.The deletion of Cg Hog1 was not releted to fungal development and virulence but resulted in enhanced sensitivity to osmotic stress and increased resistance to fludioxonil in the poplar anthracnose fungus Colletotrichum gloeosporioides.2.Under sorbitol,genes associated with glycolysis,lipid metabolism,and amino acids were differentially expressed.Among which,genes related to the synthesis of intracellular permeable substances(glycerol,soluble sugar,amino acid,betaine)were the main section.In addition,the accumulation of glycerol was not sufficient in Cg Hog1 mutant strain.It suggests that the mechanism of Cg Hog1 in response to osmotic pressure may mainly depend on the synthesis of intracellular permeable substances,especially glycerol.3.Under fludioxonil,fragmentized vacuoles occurred in the wild type whereas intact normal vacuoles were abundant in the mutant starin.In addition,vesicle trafficking-related genes were highly downregulated in the ΔCg Hog1 strain after fludioxonil treatment.Taken together,we elucidated that the mechanism of Cg Hog1 in resistance to fludioxonil may be associated with the recovery of vesical transport.In summary,we elucidated the adaptation mechanisms of how Cg Hog1 regulates appropriate response to sorbitol and fludioxonil at the transcriptome level.And these findings extend our insights into the HOG pathway in fungi. |