ABSTRACT
Biomass-derived biochar shows broad promise for persistent organic pollutants (POPs) degradation and thus establishes a more sustainable homestead. However, effective catalytic performance is still challenging. Herein, an efficient catalyst (Prussian blue decorated wood-derived biochar, PBB) was constructed by introducing Prussian blue (PB) into wood-based biochar to activate peroxymonosulfate (PMS) for removing POPs. After anchoring of PB, the degradation performance of biochar was enhanced (degradation efficiency of methylene blue (MB, 20 mg/L) increased from 52% of biochar to 95% of PBB within 60 min). The PBB presents effective MB degradation performance with a wide pH value (3.0 < pH < 11.0) or co-existing diverse anions (Cl-, NO3-, H2PO4-, and HCO3-). Electron paramagnetic resonance (EPR) analysis as well as electrochemical tests confirmed that the non-radical pathway (1O2) is the key to biochar activation of PMS, but by restricting PB into the biochar, the radical pathway (SO4â¢- and â¢OH), the non-radical pathway (1O2), and direct electron transfer can work together to activate PMS. In addition, the degradation efficiency could remain about 80% after five-time cyclic tests. This work elucidates the role of PB nanoparticles in enhancing biochar catalysts, which can inspire the development of a carbon-neutralized, cost-effective, and effective strategy for POPs removal.
Subject(s)
Environmental Pollutants , Ferrocyanides , Persistent Organic Pollutants , Wood , Charcoal/chemistry , Peroxides/chemistryABSTRACT
Rhizobia secrete effectors that are essential for the effective establishment of their symbiotic interactions with leguminous host plants. However, the signaling pathways governing rhizobial type III effectors have yet to be sufficiently characterized. In the present study, the type III effectors, NopAA and NopD, which perhaps have signaling pathway crosstalk in the regulation of plant defense responses, have been studied together for the first time during nodulation. Initial qRT-PCR experiments were used to explore the impact of NopAA and NopD on marker genes associated with symbiosis and defense responses. The effects of these effectors on nodulation were then assessed by generating bacteria in which both NopAA and NopD were mutated. RNA-sequencing analyses of soybean roots were further utilized to assess signaling crosstalk between NopAA and NopD. NopAA mutant and NopD mutant were both found to repress GmPR1, GmPR2, and GmPR5 expression in these roots. The two mutants also significantly reduced nodules dry weight and the number of nodules and infection threads, although these changes were not significantly different from those observed following inoculation with double-mutant (HH103ΩNopAA&NopD). NopAA and NopD co-mutant inoculation was primarily found to impact the plant-pathogen interaction pathway. Common differentially expressed genes (DEGs) associated with both NopAA and NopD were enriched in the plant-pathogen interaction, plant hormone signal transduction, and MAPK signaling pathways, and no further changes in these common DEGs were noted in response to inoculation with HH103ΩNopAA&NopD. Glyma.13G279900 (GmNAC27) was ultimately identified as being significantly upregulated in the context of HH103ΩNopAA&NopD inoculation, serving as a positive regulator of nodulation. These results provide new insight into the synergistic impact that specific effectors can have on the establishment of symbiosis and the responses of host plant proteins.
Subject(s)
Fabaceae , Glycine max , Glycine max/genetics , Plant Root Nodulation/genetics , Fabaceae/metabolism , Plant Roots/microbiology , Plant Proteins/metabolism , Symbiosis/geneticsABSTRACT
Soybeans (Glycine max) are a key food crop, serving as a valuable source of both oil and plant-derived protein. Pseudomonas syringae pv. glycinea (Psg) is among the most aggressive and prevalent pathogens affecting soybean production, causing a form of bacterial spot disease that impacts soybean leaves and thereby reduces crop yields. In this study, 310 natural soybean varieties were screened for Psg resistance and susceptibility. The identified susceptible and resistant varieties were then used for linkage mapping, BSA-seq, and whole genome sequencing (WGS) analyses aimed at identifying key QTLs associated with Psg responses. Candidate Psg-related genes were further confirmed through WGS and qPCR analyses. Candidate gene haplotype analyses were used to explore the associations between haplotypes and soybean Psg resistance. In addition, landrace and wild soybean plants were found to exhibit a higher degree of Psg resistance as compared to cultivated soybean varieties. In total, 10 QTLs were identified using chromosome segment substitution lines derived from Suinong14 (cultivated soybean) and ZYD00006 (wild soybean). Glyma.10g230200 was found to be induced in response to Psg, with the Glyma.10g230200 haplotype corresponding to soybean disease resistance. The QTLs identified herein can be leveraged to guide the marker-assisted breeding of soybean cultivars that exhibit partial resistance to Psg. Moreover, further functional and molecular studies of Glyma.10g230200 have the potential to offer insight into the mechanistic basis for soybean Psg resistance.