作者: Xiao-Qing Zeng , Guo-Qing Chen , Xiao-Hong Liu , Bo Dong , Huan-Bin Shi
DOI: 10.1371/JOURNAL.PONE.0103124
关键词:
摘要: The SNF1/AMPK pathway has a central role in response to nutrient stress yeast and mammals. Previous studies on SNF1 function phytopathogenic fungi mostly focused the catalytic subunit Snf1 its contribution derepression of cell wall degrading enzymes (CWDEs). However, MoSnf1 Magnaporthe oryzae was reported not be involved CWDEs regulation. mechanism how functions as virulence determinant remains unclear. In this report, we demonstrate that retains ability respond nutrient-free environment via participation peroxisomal maintenance lipid metabolism. Observation GFP-tagged targeting signal-1 (PTS1) revealed peroxisomes ΔMosnf1 were enlarged mycelia tended degraded before conidial germination, leading sharp decline amount during appressorial development, which might impart mutant great retard droplets mobilization degradation. Consequently, exhibited inability maintain normal porosity turgor pressure, are key players epidermal infection process. Exogenous glucose could partially restore ΔMosnf1. Toward further understanding pathway, β-subunit MoSip2, γ-subunit MoSnf4, two putative Snf1-activating kinases, MoSak1 MoTos3, additionally identified characterized. Here show null mutants ΔMosip2 ΔMosnf4 performed multiple disorders did, suggesting complex integrity is essential for M. kinase function. And upstream play unequal roles activation with clear preference over MoTos3. Meanwhile, lacking both them severe phenotype comparable ΔMosnf1, uncovering cooperative relationship between Taken together, our data indicate required fungal development facilitates pathogenicity by metabolism oryzae.