Guanghui Xu | PubMed Health

PubMed2026

Extreme climatic events drive consistent and predictable shifts in soil antibiotic resistance genes.

Antimicrobial resistance (AMR) is a growing One Health challenge, and as climate warming intensifies extreme events, it remains unclear how these disturbances affect soil antibiotic resistance genes (ARGs). Here we analyzed the data from a controlled experiment using soils from 30 grassland sites across ten European countries, which simulated drought, flooding, freeze-thaw, and heatwaves to explore ARG dynamics. Overall, ARGs exhibited relatively small but highly consistent shifts across treatments. Heatwaves caused the strongest reductions in ARG abundance and in their linkages with mobile genetic elements (MGEs), a pattern that may reflect a hypothesized metabolic-genetic trade-off, in which microbial investment may shift from core metabolism toward stress signaling and structural maintenance. ARG dynamics during and after disturbance were governed by distinct soil physicochemical properties, with temperature and nutrient status determining acute responses, whereas soil moisture and seasonal variability in temperature and precipitation shaped longer-term legacy effects. Cross-validated random-forest models showed positive predictive performance for Bray-Curtis-based compositional responses within the environmental range represented by the 30 grassland sites. Our findings enhance the understanding of how soil ARGs respond to extreme climatic events and provide a step toward predicting extreme-event impacts on soil resistomes with relevance to One Health.

Soil Microbiology↗

PubMed2026

Chromatin Remodeling Subunit ARID1A Negatively Regulates the Malignant Progression of Gastrointestinal Stromal Tumors by Targeting the MEMO1 Promoter.

Gastrointestinal stromal tumors (GISTs) are the most common sarcomas of the alimentary tract and are primarily characterized by malignant progression, a major cause of mortality. AT-rich interaction domain 1A (ARID1A), a core component of the chromatin-remodeling SWI/SNF complex, has been found to correlate with GIST tumor grade, although the underlying mechanism remains unclear. Its frequent inactivation across diverse cancer types reveals pleiotropic roles that intersect multiple hallmarks of cancer. In this study, we aimed to investigate the potential relationship between ARID1A and malignant progression in GISTs, as well as the underlying mechanism. Western blotting, real-time polymerase chain reaction, and immunohistochemistry were used to assess ARID1A expression in GIST tissues. Cell Counting Kit-8 (CCK-8) assays were performed to evaluate cell proliferation. Wound-healing and Transwell assays were conducted to assess cell migration and invasion. Flow cytometry was used to analyze apoptosis and cell cycle distribution. Label-free quantitative proteomics and chromatin immunoprecipitation sequencing (ChIP-seq) were employed to identify top candidate downstream targets of ARID1A. ARID1A expression was decreased in high-risk GIST tissues. Furthermore, ARID1A knockdown in GIST cells promoted proliferation and metastasis both in vitro and in vivo, and led to reduced apoptosis and impaired cell cycle arrest. We further demonstrated that ARID1A suppresses GIST proliferation and metastasis by inhibiting MEMO1 expression and inactivating the ERK1/2 signaling pathway. Notably, this regulatory axis was observed in KIT-null GIST cells, indicating that the ARID1A-MEMO1 pathway may function independently of canonical KIT signaling. Thus, ARID1A inhibits malignant progression in GISTs, providing new insights into its role in the prevention and treatment of human GISTs and suggesting its potential as a biomarker of malignant progression in GISTs.

Humans↗