Salinity stress severely limits crop productivity worldwide. While plant growth-promoting rhizobacteria (PGPR) are known to alleviate abiotic stress, the specific mechanisms mediated by their volatile organic compounds (VOCs) remain largely elusive. In this study, an in vitro split-plate system was used to investigate the effects of VOCs emitted by Bacillus velezensis SQR9 on Arabidopsis thaliana seedlings under salt stress. Exposure to SQR9 VOCs significantly enhanced Arabidopsis salt tolerance, evidenced by increased biomass and root growth. Mechanistically, SQR9 VOCs mitigated salt-induced damage by increasing chlorophyll content, modulating osmolytes, and reducing malondialdehyde (MDA) levels. SQR9 VOCs alleviated oxidative stress by decreasing ROS (H₂O₂, O₂⁻) accumulation and enhancing antioxidant enzyme (SOD, CAT, POD) activities. Furthermore, SQR9 VOCs maintained ion homeostasis by significantly reducing leaf Na⁺ accumulation, maintaining a high K⁺/Na⁺ ratio, and upregulating key ion transporter genes. Analysis of the headspace from SQR9 cultured on MSgg medium identified 2,3-butanediol (2,3-BD) as a major active VOC. Exogenous application of 2,3-BD successfully mimicked the growth-promoting and salt-tolerance-enhancing effects of SQR9. Our findings demonstrate that SQR9 VOCs, particularly 2,3-BD, systemically prime Arabidopsis for salt tolerance by co-activating the antioxidant defense system and the SOS ion homeostasis pathway.

Microcystin (MC) risk is often assessed within bloom-affected lakes and reservoirs, although hydrological connectivity can extend exposure into downstream river and estuarine networks. We synthesize evidence using a lake–river continuum framework that treats connected reaches as active processing environments. The framework separates the source pool, export flux, and downstream exposure, and distinguishes advective redistribution, reversible retention, irreversible transformation, and source or remobilization processes. Hydrology sets reaction opportunity, while phase partitioning, photochemical and microbial transformation, sediment exchange, and biological uptake determine how MC mass and bioavailability change during transport. Field evidence shows that downstream occurrence cannot be inferred reliably from visible source blooms: reaches may attenuate, retain, redistribute, or locally renew MC exposure depending on hydraulic state and process coupling. These dynamics shift exposure among water, particles, sediments, cells, and biota. Consequently, source-lake indicators or water concentrations alone can mischaracterize ecological exposure, and drinking-water guideline values are not ecological protection thresholds. Key priorities are flux-resolved monitoring, direct field estimates of process rates and transformation products, chronic ecotoxicology matched to realistic exposure routes, and hierarchical transport–biogeochemical models. This continuum perspective links source, process, pathway, receptor, and effect within a single source-to-risk framework.