Metal oxide nanoparticles inhibit nitrogen fixation and rhizosphere colonization by inducing ROS in associative nitrogen-fixing bacteria Pseudomonas stutzeri A1501.

The potential effects of engineered metal oxide nanoparticles (MONPs) on bacterial nitrogen fixation are of great concern. Herein, the impact and mechanism of the increasing-used MONPs, including TiO2, Al2O3, and ZnO nanoparticles (TiO2NP, Al2O3NP, and ZnONP, respectively), on nitrogenase activity was studied at the concentrations ranging from 0 to 10 mg L-1 using associative rhizosphere nitrogen-fixing bacteria Pseudomonas stutzeri A1501. Nitrogen fixation capacity was inhibited by MONPs in an increasing degree of TiO2NP < Al2O3NP < ZnONP. Realtime qPCR analysis showed that the expressions of nitrogenase synthesis-related genes, including nifA and nifH, were inhibited significantly when MONPs were added. MONPs could cause the explosion of intracellular ROS, and ROS not only changed the permeability of the membrane but also inhibited the expression of nifA and biofilm formation on the root surface. The repressed nifA gene could inhibit transcriptional activation of nif-specific genes, and ROS reduced the biofilm formation on the root surface which had a negative effect on resisting environmental stress. This study demonstrated that MONPs, including TiO2NP, Al2O3NP, and ZnONP, inhibited bacterial biofilm formation and nitrogen fixation in the rice rhizosphere, which might have a negative effect on the nitrogen cycle in bacteria-rice system.

An orphan protein of Fusarium graminearum modulates host immunity by mediating proteasomal degradation of TaSnRK1α.

Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein (OSP) genes of F. graminearum. Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions.

Independent losses and duplications of autophagy-related genes in fungal tree of life.

Autophagy is important for growth, development and pathogenesis in fungi. Although autophagic process is generally considered to be conserved, the conservation and evolution of ATG genes at kingdom-wide remains to be conducted. Here we systematically identified 41 known ATG genes in 331 species and analyzed their distribution across the fungal kingdom. In general, only 20 ATG genes are highly conserved, including most but not all the yeast core-autophagy-machinery genes. Four functional protein groups involved in autophagosome formation had conserved and non-conserved components, suggesting plasticity in autophagosome formation in fungi. All or majority of the key ATG genes were lost in several fungal groups with unique lifestyles and niches, such as Microsporidia, Pneumocystis and Malassezia. Moreover, majority of ATG genes had A-to-I RNA editing during sexual reproduction in two ascomycetes and deletion of FgATG11, the ATG gene with the most editing sites in Fusarium affected ascospore releasing. Duplication and divergence also was observed to several core ATG genes, such as highly divergent ATG8 paralogs in dermatophytes and multiple ATG15 duplications in mushrooms. Taken together, independent losses and duplications of ATG genes have occurred throughout the fungal kingdom and variations in autophagy exist among different lineages and possibly different developmental stages.