Systemic studies on the effects of mitogen-activated protein kinase （MAPK） signal transduction pathway on the growth and development of Setosphaeria turcica is helpful not only in understanding the molecular mechani...Systemic studies on the effects of mitogen-activated protein kinase （MAPK） signal transduction pathway on the growth and development of Setosphaeria turcica is helpful not only in understanding the molecular mechanism of pathogenhost interaction but also in the effective control of the diseases caused by S. turcica. U0126, the specific MEK inhibitor, is used to treat S. turcica before the observation of the conidial germination, appressorium production, and pathogenicity of the pathogen. There is no significant effect of U0126 on the colony morphology and mycelium growth of the pathogen. After treatment with U0126, the growth of mycelium and conidia are normal, but the conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are significantly inhibited. Under the definite concentration scope, an increase in U0126 concentration increases the inhibition degree of conidial germination and appressorium production, but the inhibition degree decreases with elongation of treatment time. The conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are regulated by the MAPK pathway inhibited by U0126.展开更多
Rice false smut,which is caused by Ustilaginoidea virens,is an emerging disease of rice spikelets in rice-growing areas worldwide.However,the infection mechanism of U.virens on rice spikelets is still unclear.Here,we ...Rice false smut,which is caused by Ustilaginoidea virens,is an emerging disease of rice spikelets in rice-growing areas worldwide.However,the infection mechanism of U.virens on rice spikelets is still unclear.Here,we characterized a suppressor of mitogen-activated protein kinase kinase or ERK kinase(MEK)null(UvSMEKI)in U.virens that is conserved among filamentous fungi.Compared with wild type U.virens strain P-1,UvSMEKI deletion mutants were defective in pathogenicity and conidial germination.In addition,conidiation of UvSMEKI deletion mutants was significantly reduced on yeast extract tryptone(YT)plates,but inc「eased in YT broth compared with the wild type.Compared with UvSMEKI expression level during the vegetative mycelia and conidiation stages,UvSMEKI dramatically increased during infection of rice florets.Surprisingly,the UvSMEKI deletion mutants exhibited higher tolerance to H_(2)O_(2) and NaCl.In summary,presented evidence suggested that UvSMEKI positively regulated pathogenicity,conidial germination and conidiation in YT broth,and negatively regulated conidiation on YT medium and tolerance to oxidative and osmotic stresses.The results enhanee our understanding of the regulatory mechanism of pathogenicity of U.virens,and present a potential molecular target for blocking rice infection by U.virens.展开更多
基金supported by the National Natural Science Foundation of China(30471126)Doctoral Foundation Project of Hebei Province,China(05547007D-2).
文摘Systemic studies on the effects of mitogen-activated protein kinase （MAPK） signal transduction pathway on the growth and development of Setosphaeria turcica is helpful not only in understanding the molecular mechanism of pathogenhost interaction but also in the effective control of the diseases caused by S. turcica. U0126, the specific MEK inhibitor, is used to treat S. turcica before the observation of the conidial germination, appressorium production, and pathogenicity of the pathogen. There is no significant effect of U0126 on the colony morphology and mycelium growth of the pathogen. After treatment with U0126, the growth of mycelium and conidia are normal, but the conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are significantly inhibited. Under the definite concentration scope, an increase in U0126 concentration increases the inhibition degree of conidial germination and appressorium production, but the inhibition degree decreases with elongation of treatment time. The conidial germination, appressorium production, and pathogenicity of S. turcica on susceptible corn leaves are regulated by the MAPK pathway inhibited by U0126.
基金supported by the National Key Research and Development Project in China(Grant No.2016YFD200805)National Natural Science Foundation of China(Grant Nos.31301624 and 31571961).
文摘Rice false smut,which is caused by Ustilaginoidea virens,is an emerging disease of rice spikelets in rice-growing areas worldwide.However,the infection mechanism of U.virens on rice spikelets is still unclear.Here,we characterized a suppressor of mitogen-activated protein kinase kinase or ERK kinase(MEK)null(UvSMEKI)in U.virens that is conserved among filamentous fungi.Compared with wild type U.virens strain P-1,UvSMEKI deletion mutants were defective in pathogenicity and conidial germination.In addition,conidiation of UvSMEKI deletion mutants was significantly reduced on yeast extract tryptone(YT)plates,but inc「eased in YT broth compared with the wild type.Compared with UvSMEKI expression level during the vegetative mycelia and conidiation stages,UvSMEKI dramatically increased during infection of rice florets.Surprisingly,the UvSMEKI deletion mutants exhibited higher tolerance to H_(2)O_(2) and NaCl.In summary,presented evidence suggested that UvSMEKI positively regulated pathogenicity,conidial germination and conidiation in YT broth,and negatively regulated conidiation on YT medium and tolerance to oxidative and osmotic stresses.The results enhanee our understanding of the regulatory mechanism of pathogenicity of U.virens,and present a potential molecular target for blocking rice infection by U.virens.
