Whole-genome sequencing of Fusarium spp. causing sugarcane root rot on both chewing cane and sugar-making cane.

Previously we isolated three Fusarium strains (a F. sacchari strain namely GXUF-1, and another two F. commune strains namely GXUF-2 and GXUF-3), and we verified that GXUF-3 was able to cause sugarcane root rot to the chewing cane cultivar Badila. Considering that Fusarium spp. are a group of widely distributed fungal pathogens, we tested whether these three Fusarium isolates were able to cause root rot to Badila as well as sugar-making cane cultivar (Guitang42), using a suitable inoculation method established based on infection assays using Badila. We found that the three Fusarium strains were able to cause root rot symptoms to both Badila and Guitang42, to different extents. To better investigate the potential pathogenicity mechanisms, we performed Illumina high-throughput sequencing and analyzed the whole genomic sequence data of these three Fusarium strains. The results reveal that the assembly sizes of the three Fusarium strains were in a range of 44.7-48.2 Mb, with G + C contents of 48.0-48.5%, and 14,154-15,175 coding genes. The coding genes were annotated by multiple public databases, and potential pathogenic genes were predicted using proprietary databases (such as PHI, DFVF, CAZy, etc.). Furthermore, based on evolutionary analysis of the coding sequence, we found that contraction and expansion of gene families occurred in the three Fusarium strains. Overall, our results suggest a potential risk that the root rot disease may occur to the sugar-making canes although it was initially spotted from fruit cane, and provide clues to understand the pathogenic mechanisms of Fusarium spp. causing sugarcane root rot.

Soil pH restricts the ability of biochar to passivate cadmium: A meta-analysis.

Soil acidification is the main cause for aggravation of soil cadmium (Cd) pollution. Biochar treatment can increase the soil pH and decrease the Cd availability in soils. However, there is limited information in literature on the comprehensive assessment of the response of Cd fractions to biochar. Therefore, in the present meta-analysis study, we evaluate the response of Cd fractions to biochar application in soils with different pH and to further examine the effect of physicochemical properties of biochar on Cd. Results from the overall analysis indicated that biochar treatment increased the soil pH by 7.0%, thereby decreasing the amount of available Cd (37.3%). In acidic soil, biochar significantly reduced the acid-soluble fraction (Acid-Cd) of Cd by 36.8%, while Oxidizable fraction of Cd (Oxid-Cd, 20.9%) and Residual fraction of Cd (Resid-Cd, 22.2%) were significantly increased. In neutral soils, only Acid-Cd was significantly reduced (33.0%) in the presence of biochar. In alkaline soils, biochar caused significant reduction in Acid-Cd of 12.4% and an increase in Oxid-Cd and Resid-Cd of 26.6% and 47.8%, respectively. Further, our findings showed that biochar with cation exchange capacity >100 cmol+/kg effectively decreased Acid-Cd (32.4%), while biochar with the percentage of hydrogen <2% was more contributory in increasing Resid-Cd (64.3%). These results demonstrate the importance of soil pH in regulating the biological effectiveness of Cd in soil and the complexation between the functional groups of biochar and Cd, and provide key information for the remediation of Cd pollution in soils with different pH by biochar.

TIGAR/AP-1 axis accelerates the division of Lgr5- reserve intestinal stem cells to reestablish intestinal architecture after lethal radiation.

During radiologic or nuclear accidents, high-dose ionizing radiation (IR) can cause gastrointestinal syndrome (GIS), a deadly disorder that urgently needs effective therapy. Unfortunately, current treatments based on natural products and antioxidants have shown very limited effects in alleviating deadly GIS. Reserve intestinal stem cells (ISCs) and secretory progenitor cells are both reported to replenish damaged cells and contribute to crypt regeneration. However, the suppressed ß-catenin/c-MYC axis within these slow-cycling cells leads to limited regenerative response to restore intestinal integrity during fatal accidental injury. Current study demonstrates that post-IR overexpression of TIGAR, a critical downstream target of c-MYC in mouse intestine, mounts a hyperplastic response in Bmi1-creERT+ reserve ISCs, and thus rescues mice from lethal IR exposure. Critically, by eliminating damaging reactive oxygen species (ROS) yet retaining the proliferative ROS signals, TIGAR-overexpression enhances the activity of activator protein 1, which is indispensable for initiating reserve-ISC division after lethal radiation. In addition, it is identified that TIGAR-induction exclusively gears the Lgr5- subpopulation of reserve ISCs to regenerate crypts, and intestinal TIGAR-overexpression displays equivalent intestinal reconstruction to reserve-ISC-restricted TIGAR-induction. Our findings imply that precise administrations toward Lgr5- reserve ISCs are promising strategies for unpredictable lethal injury, and TIGAR can be employed as a therapeutic target for unexpected radiation-induced GIS.

New molecular insights into the tyrosyl-tRNA synthase inhibitors: CoMFA, CoMSIA analyses and molecular docking studies.

Drug resistance caused by excessive and indiscriminate antibiotic usage has become a serious public health problem. The need of finding new antibacterial drugs is more urgent than ever before. Tyrosyl-tRNA synthase was proved to be a potent target in combating drug-resistant bacteria. In silico methodologies including molecular docking and 3D-QSAR were employed to investigate a series of newly reported tyrosyl-tRNA synthase inhibitors of furanone derivatives. Both internal and external cross-validation were conducted to obtain high predictive and satisfactory CoMFA model (q 2 = 0.611, r 2pred = 0.933, r 2m = 0.954) and CoMSIA model (q 2 = 0.546, r 2pred = 0.959, r 2m = 0.923). Docking results, which correspond with CoMFA/CoMSIA contour maps, gave the information for interactive mode exploration. Ten new molecules designed on the basis of QSAR and docking models have been predicted more potent than the most active compound 3-(4-hydroxyphenyl)-4-(2-morpholinoethoxy)furan-2(5H)-one (15) in the literatures. The results expand our understanding of furanones as inhibitors of tyrosyl-tRNA synthase and could be helpful in rationally designing of new analogs with more potent inhibitory activities.