Glyphosate has emerged as the most widespread herbicide to control annual and perennial weeds. Massive use of glyphosate for decades has resulted in its ubiquitous presence in the environment, and poses a threat to humans and ecosystem. Different approaches such as adsorption, photocatalytic degradation, and microbial degradation have been studied to break down glyphosate in the environment. Among these, microbial degradation is the most effective and eco-friendly method. During its degradation, various microorganisms can use glyphosate as a sole source of phosphorus, carbon, and nitrogen. Major glyphosate degradation pathways and its metabolites have been frequently investigated, but the related enzymes and genes have been rarely studied. There are many reviews about the toxicity and fate of glyphosate and its major metabolite, aminomethylphosphonic acid. However, there is lack of reviews on biodegradation and bioremediation of glyphosate. The aims of this review are to summarize the microbial degradation of glyphosate and discuss the potential of glyphosate-degrading microorganisms to bioremediate glyphosate-contaminated environments. This review will provide an instructive direction to apply glyphosate-degrading microorganisms in the environment for bioremediation.

Persistent use of permethrin has resulted in its ubiquitous presence as a contaminant in surface streams and soils, yet little is known about the kinetics and metabolic behaviors of this pesticide. In this study, a novel bacterial strain Acinetobacter baumannii ZH-14 utilizing permethrin via partial hydrolysis pathways was isolated from sewage sludge. Response surface methodology based on Box-Behnken design of cultural conditions was used for optimization resulting in 100% degradation of permethrin (50 mg·L−1) within 72 h. Strain ZH-14 degraded permethrin up to a concentration of 800 mg·L−1. Biodegradation kinetics analysis indicated that permethrin degradation by this strain was concentration dependent, with a maximum specific degradation rate, half-saturation constant, and inhibition constant of 0.0454 h−1, 4.7912 mg·L−1, and 367.2165 mg·L−1, respectively. High-performance liquid chromatography and gas chromatography-mass spectrometry identified 3-phenoxybenzenemethanol and 3-phenoxybenzaldehyde as the major intermediate metabolites of the permethrin degradation pathway. Bioaugmentation of permethrin-contaminated soils with strain ZH-14 significantly enhanced degradation, and over 85% of permethrin was degraded within 9 days with the degradation process following the first-order kinetic model. In addition to degradation of permethrin, strain ZH-14 was capable of degrading a large range of synthetic pyrethroids such as deltamethrin, bifenthrin, fenpropathrin, cyhalothrin, and beta-cypermethrin which are also widely used pesticides with environmental contamination problems, suggesting the promising potentials of A. baumannii ZH-14 in bioremediation of pyrethroid-contaminated terrestrial and aquatic environments.

Quorum quenching (QQ) is a promising strategy for preventing and controlling quorum sensing (QS)-mediated bacterial infections. It interferes with QS by the inhibition of signal synthesis, the detection of enzyme-catalyzed degradation, and the modification of signals. N-Acyl homoserine lactones (AHLs) represent a family of widely conserved QS signals involved in the regulation of virulence factor production in many Gram-negative bacterial pathogens. In this study, AHL-degrading bacterial strains were isolated, and the most efficient one was evaluated for its potential against QS-mediated pathogens. Results showed that an AHL-degrading bacteria Ochrobactrum intermedium D-2 effectively attenuated maceration produced by the pathogen Pectobacterium carotovorum subsp. carotovorum (Pcc) on radish and potato slices. Strain D-2 exhibited a superior AHL degradation activity and efficiently degraded various AHLs, including N-hexanoyl-L-homoserine lactone (C6HSL), N-(3-oxohexanoyl)-L-homoserine lactone (3OC6HSL), N-(3-oxooctanoyl)-L-homoserine lactone (3OC8HSL), and N-(3-oxododecanoyl)-L-homoserine lactone (3OC12HSL). Analysis of the degradation products of AHL by gas chromatography-mass spectrometry led to the identification of N-cyclohexyl-propanamide and propanamide as the main intermediate products, suggesting that AHL was degraded by hydrolysis. Annotation and analysis of the whole genome sequence of strain D-2 revealed the presence of an AHL-lactonase, termed AidF. Moreover, the application of strain D-2 was able to substantially reduce the disease severity caused by Pcc on host plants. These results reveal the biochemical basis of a highly efficient AHL-degrading bacterial isolate and present the potential to attenuate Pcc virulence through QQ.

Diffusible signal factor (DSF) represents a family of widely conserved quorum sensing (QS) signals involved in the regulation of virulence factor production in many Gram-negative bacterial pathogens. Quorum quenching, which disrupts QS either by degradation of QS signals or interference of signal generation or perception, is a promising strategy for prevention and control of QS-mediated bacterial infections. In this study, a novel DSF-degrading strain, HN-2, was isolated from contaminated soil and identified as Cupriavidus sp. The isolate exhibited superior DSF degradation activity and completely degraded 2 mmol·L–1 of DSF within 24 h. Analysis of the degradation products of DSF by gas chromatography–mass spectrometry led to the identification of trans-2-decenoic acid methyl ester as the main intermediate product, suggesting that DSF could be degraded by oxidation and hydroxylation. Moreover, this study presents for the first time, evidence that Cupriavidus sp. can reduce the black rot disease caused by Xanthomonas campestris pv. campestris (Xcc). Application of the HN-2 strain as a biocontrol agent could substantially reduce the disease severity. These findings reveal the biochemical basis of a highly efficient DSF-degrading bacterial isolate and present a useful agent for controlling infectious diseases caused by DSF-dependent bacterial pathogens.