The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) has been widely used around the world in both agricultural and non-agricultural fields due to its high activity. However, the heavy use of 2,4-D has resulted in serious environmental contamination, posing a significant risk to non-target organisms, including human beings. This has raised substantial concerns regarding its impact. In addition to agricultural use, accidental spills of 2,4-D can pose serious threats to human health and the ecosystem, emphasizing the importance of prompt pollution remediation. A variety of technologies have been developed to remove 2,4-D residues from the environment, such as incineration, adsorption, ozonation, photodegradation, the photo-Fenton process, and microbial degradation. Compared with traditional physical and chemical remediation methods, microorganisms are the most effective way to remediate 2,4-D pollution because of their rich species, wide distribution, and diverse metabolic pathways. Numerous studies demonstrate that the degradation of 2,4-D in the environment is primarily driven by enzymatic processes carried out by soil microorganisms. To date, a number of bacterial and fungal strains associated with 2,4-D biodegradation have been isolated, such as Sphingomonas, Pseudomonas, Cupriavidus, Achromobacter, Ochrobactrum, Mortierella, and Umbelopsis. Moreover, several key enzymes and genes responsible for 2,4-D biodegradation are also being identified. However, further in-depth research based on multi-omics is needed to elaborate their role in the evolution of novel catabolic pathways and the microbial degradation of 2,4-D. Here, this review provides a comprehensive analysis of recent progress on elucidating the degradation mechanisms of the herbicide 2,4-D, including the microbial strains responsible for its degradation, the enzymes participating in its degradation, and the associated genetic components. Furthermore, it explores the complex biochemical pathways and molecular mechanisms involved in the biodegradation of 2,4-D. In addition, molecular docking techniques are employed to identify crucial amino acids within an alpha-ketoglutarate-dependent 2,4-D dioxygenase that interacts with 2,4-D, thereby offering valuable insights that can inform the development of effective strategies for the biological remediation of this herbicide.

Quorum sensing (QS) is a communication mechanism used among microorganisms that regulate the population density and behavior by sensing the concentration of signaling molecules. Quorum quenching (QQ), a novel, eco-friendly, and efficient method for disease control, interferes with QS by disturbing the production and enzymatic degradation of signaling molecules, blocking communication among microorganisms, and thus has deep potential for use in plant disease control. Pectobacterium carotovorum can cause bacterial soft rot, resulting in yield reduction in a variety of crops worldwide, and can be mediated and regulated by the N-acyl homoserine lactones (AHLs), which are typical signaling molecules. In this study, a novel quenching strain of Pseudomonas multiresinivorans QL-9a was isolated and characterized, and it showed excellent degradation ability against AHLs, degrading 98.20% of N-(-3-oxohexanoyl)-L-homoserine lactone (OHHL) within 48 h. Based on the results of the gas chromatography–mass spectrometer (GC–MS) analysis, a possible pathway was proposed to decompose OHHL into fatty acids and homoserine lactone, in which AHL acylase was involved. Additionally, it has been demonstrated that the QL-9a strain and its crude enzyme are promising biocontrol agents that can considerably reduce the severity of the soft rot disease brought on by P. carotovorum, consequently preventing the maceration of a variety of host plant tissues. All of these results suggest promising applications of the QL-9a strain and its crude enzyme in the control of various plant diseases mediated by AHLs.

Quorum sensing (QS) is critically involved in mediating microbial interactions and serves as a central regulatory mechanism in bacterial pathogenesis. As an emerging countermeasure, quorum quenching (QQ) suppresses QS-regulated virulence through enzymatic or chemical disruption of signal systems. N-acyl homoserine lactone (AHL), an evolutionarily conserved QS signal, coordinates the pathogenicity of multiple plant pathogens, particularly Dickeya zeae, which causes soft rot disease in various crops and leads to substantial agricultural losses. In this study, the QQ strain Acinetobacter schindleri XJ-10 was evaluated for its capacity to degrade AHL and attenuate the pathogenicity of D. zeae EC1 in host plants. Notably, strain XJ-10 exhibited efficient AHL degradation at 0.2 mmol/L within 24 h, achieving a degradation efficiency of 98.80%. Subsequently, gas chromatography–mass spectrometry (GC-MS) analysis identified N-hexanoyl-L-homoserine lactone and propanamide as key intermediates during AHL degradation, confirming complete mineralization to CO₂ and H₂O. Based on the structural characterization of AHL and its intermediates, the metabolic pathway within strain XJ-10 was proposed. The degradation pathway initiates with the hydrolysis of the ester ring of N-hexanoyl-L-homoserine lactone, generating N-hexanoyl-L-homoserine. Subsequent carbon–nitrogen bond scission is predicted to yield N-cyclohexyl-propanamide, which is further catabolized to produce hexanamide and propanamide. Furthermore, strain XJ-10 exhibited biocontrol activity against soft rot disease affecting potato (Solanum tuberosum), radish (Raphanus sativus), and Chinese cabbage (Brassica rapa subsp. pekinensis), as its crude enzyme extract effectively reduced disease incidence and severity in planta. While strain XJ-10 showed no detectable acylase activity, it exhibited significant degradation activity against AHL, suggesting a distinct QQ mechanism. Collectively, these findings broaden the scope of QQ-based biocontrol strategies and enhance mechanistic insights into managing bacterial diseases through QS modulation.