Search

BACKGROUND Understanding the specific inhibitory effects of different Brassica seed meals (BSMs) on soilborne pathogens is important for their application as biocontrol agents for controlling plant disease. In this study, the seed meals of Brassica napus L. (BnSM), Brassica campestris L. (BcSM), and Brassica juncea L. (BjSM), and the combined seed meal of BcSM and BjSM (CSM, 1:1), were selected for investigation. The inhibitory effects of these seed meals on the plant pathogen Ralstonia solanacearum (Smith) and tomato bacterial wilt, were assessed and compared. RESULTS: All the BSMs significantly inhibited the growth of R. solanacearum in vitro. Furthermore, the BSMs could effectively suppress R. solanacearum virulence traits, including motility, exopolysaccharide production, dehydrogenase activity, virulence‐related gene expression, and colonization in the soil. Among them, BjSM showed the best inhibiting effects, and CSM displayed synergic toxicity against R. solanacearum. In addition, the predominant antibacterial compounds in BcSM and BjSM were identified as the volatile compounds, 3‐butenyl isothiocyanate and allyl isothiocyanate, respectively. Finally, pot experiment verified that the control effects of BjSM and CSM on tomato wilt reached more than 90%. CONCLUSION: This is the first study to report on the ability of different kinds of BSMs to suppress the virulence of R. solanacearum and biocontrol efficiencies against bacterial wilt in tomato plants. Furtherly, the main antibacterial compounds in the BSMs were identified. The results demonstrated that CSM may possess potential for controlling bacterial wilt caused by R. solanacearum. The results provide a fresh perspective for comprehending the mechanism underlying BSM suppression of pathogens and plant disease. [ABSTRACT FROM AUTHOR]

Importance: Assembling a functional microbial consortium and identifying key degraders involved in the degradation of 1,4-dioxane are crucial for the design of synergistic consortia used in enhancing the bioremediation of 1,4-dioxane-contaminated sites. However, due to the vast diversity of microbes, assembling a functional consortium and identifying novel degraders through a simple method remain a challenge. In this study, we reassembled 1,4-dioxane-degrading microbial consortia using a simple and easy-to-operate method by combining dilution-to-extinction and reculture techniques. We combined differential analysis of community structure and metabolic function and confirmed that Shinella species have a stronger 1,4-dioxane degradation ability than Xanthobacter species in the enriched consortium. In addition, a new dioxane-degrading bacterium was isolated, Shinella yambaruensis , which verified our findings. These results demonstrate that DTE and reculture techniques can be used beyond diversity reduction to assemble functional microbial communities, particularly to identify key degraders in contaminant-degrading consortia., Competing Interests: The authors declare no conflict of interest.

Somatic mutation of isocitrate dehydrogenase 1 (IDH1) is now recognized as the most common initiating event for secondary glioblastoma, a brain tumor type arising with high frequency in the frontal lobe. A puzzling feature of IDH1 mutation is the selective manifestation of glioma as the only neoplasm frequently associated with early postzygotic occurrence of this genomic alteration. We report here that IDH1(R132H) exhibits a growth-inhibitory effect that is abrogated in the presence of glutamate dehydrogenase 2 (GLUD2), a hominoid-specific enzyme purportedly optimized to facilitate glutamate turnover in human forebrain. Using murine glioma progenitor cells, we demonstrate that IDH1(R132H) exerts a growth-inhibitory effect that is paralleled by deficiency in metabolic flux from glucose and glutamine to lipids. Examining human gliomas, we find that glutamate dehydrogenase 1 (GLUD1) and GLUD2 are overexpressed in IDH1-mutant tumors and that orthotopic growth of an IDH1-mutant glioma line is inhibited by knockdown of GLUD1/2. Strikingly, introduction of GLUD2 into murine glioma progenitor cells reverses deleterious effects of IDH1 mutation on metabolic flux and tumor growth. Further, we report that glutamate, a substrate of GLUD2 and a neurotransmitter abundant in mammalian neocortex, can support growth of glioma progenitor cells irrespective of IDH1 mutation status. These findings suggest that specialization of human neocortex for high glutamate neurotransmitter flux creates a metabolic niche conducive to growth of IDH1 mutant tumors.

In the title complex, [Mn(C(16)H(14)N(4)O)(C(2)H(5)OH)(2)(H(2)O)](C(6)H(2)N(3)O(7))(2)·2C(2)H(5)OH, the Mn(II) ion is in a distorted octa-hedral coordination environment, defined by an MnN(2)O(4) donor set. The 1,3-bis-(benz-imid-azol-2-yl)-2-oxapropane ligand is tridentate. In the crystal structure, inter-molecular N-H⋯O and O-H⋯O hydrogen bonds link the components into a three-dimensional network. The O atoms of one of the nitro groups are disordered over two sets of sites with refined occupancies of 0.577 (11) and 0.423 (11).