Soil salinization, an overwhelming problem exacerbated by climate change and anthropogenic activities, poses a significant threat to global food security by impairing plant growth, development, and crop productivity. Salinity stress induces osmotic, ionic, and oxidative stresses, disrupting physiological and biochemical processes in plants. Anthocyanins, a class of flavonoids, have emerged as key players in mitigating salt stress through their antioxidant properties, ROS scavenging, and regulation of stress-responsive pathways. During salt stress, ROS act as damaging agents and signaling molecules, upregulating anthocyanin-related genes to mitigate oxidative stress and maintain cellular homeostasis. Anthocyanins mitigate salt stress by regulating osmotic balance, ion homeostasis, and antioxidant defenses. Their biosynthesis is regulated by a network of structural and regulatory genes, including MYB, bHLH, and WD40 transcription factors, influenced by epigenetic modifications and hormonal signaling pathways such as ABA, JA, and SA. Advances in genetic engineering, including CRISPR/Cas9-mediated gene editing, have enabled the development of anthocyanin-rich transgenic plants with enhanced salt tolerance. For instance, transgenic plants overexpressing anthocyanin biosynthesis genes like DFR and ANS have demonstrated enhanced salt tolerance in crops such as tomatoes and rice. However, challenges such as variability in anthocyanin accumulation and stability under environmental stressors remain. This review highlights the translational potential of anthocyanins in crop improvement, emphasizing the need for integrated multi-omics approaches and field trials to validate their efficacy. By elucidating the molecular mechanisms of salt stress and anthocyanin-mediated stress alleviation, this work provides a foundation for developing resilient crops to address the growing challenges of soil salinization.

Fluoride, a naturally occurring element found in water, soil, food, and atmospheric precipitation, can lead to fluorosis and various health issues when consumed excessively. However, the mechanism of fluorosis is still under investigation. This study utilizes Caenorhabditis elegans as a model organism to investigate the effects of fluoride exposure on biological systems and to explore the mechanisms by which curcumin mitigates fluoride- induced toxicity. Three groups were established: a blank control, a sodium fluoride (NaF) exposure group (concentration 5 mmol/L), and a curcumin intervention group (concentration 25 mu mol/L). Physiological parameters, lipofuscin levels, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, and mitochondrial copy numbers were measured to assess the effects of fluoride toxicity and curcumin protection. RNA-seq and qRT-PCR were utilized to investigate the molecular mechanisms underlying fluoride- induced damage and curcumin's mitigating effects. Results indicated that fluoride-exposed nematodes displayed physiological abnormalities, increased ROS production, higher lipofuscin levels, altered mitochondrial membrane potential and mitochondrial copy number, and activated MAPK signaling pathway genes. Curcumin exhibited protective effects on these parameters, suggesting its potential in preventing fluoride-induced harm by modulating oxidative stress and preserving mitochondrial function. This research enhances our understanding of the mechanisms of fluoride toxicity and highlights the potential benefits of curcumin.

Introduction: Research on Glycyrrhiza uralensis, a nonhalophyte that thrives in saline-alkaline soil and a traditional Chinese medicinal component, is focused on improving its ability to tolerate salt stress to increase its productivity and preserve its Dao-di characteristics. Furthermore, the inoculation of bioagents such as Bacillus subtilis to increase plant responses to abiotic stressors is currently a mainstream strategy. Mitogen-activated protein kinase (MAPK), a highly conserved protein kinase, plays a significant role in plant responses to various abiotic stress pathways. Methods: This investigation involved the identification of 21 members of the GuMAPK family from the genome of G. uralensis, with an analysis of their protein conserved domains, gene structures, evolutionary relationships, and phosphorylation sites using bioinformatics tools. Results: Systematic evolutionary analysis of the 21 GuMAPKs classified them into four distinct subgroups, revealing significant differences in gene structure and exon numbers. Collinearity analysis highlighted the crucial role of segmental duplication in expanding the GuMAPK gene family, which is particularly evident in G. uralensis and shows a close phylogenetic relationship with Arabidopsis thaliana, tomato, and cucumber. Additionally, the identification of phosphorylation sites suggests a strong correlation between GuMAPK and various physiological processes, including hormonal responses, stress resistance, and growth and development. Protein interaction analysis further supported the role of GuMAPK proteins in regulating essential downstream genes. Through examination of transcriptome expression patterns, GuMAPK16-2 emerged as a prospective pivotal regulatory factor in the context of salt stress and B. subtilis inoculation, a finding supported by its subcellular localization within the nucleus. Discussion: These discoveries offer compelling evidence for the involvement of GuMAPK in the salt stress response and for the exploration of the mechanisms underlying B. subtilis' enhancement of salt tolerance in G. uralensis.

Chlorothalonil (CTL) is widely used in agricultural production and antifoulant additive globally due to its broad spectrum and non-systemic properties, resulting in its widespread existence in foods, soil and water. Extensive evidence demonstrated that exposure to CTL induced adverse effects on organisms and in particular its reproductive toxicity has been attracted public concern. However, the influences of CTL on oocyte maturation is mysterious so far. In this study, we documented the toxic effects of CTL on oocyte in vitro maturation and the related underlying mechanisms. Exposure to CTL caused continuous activation of spindle assembly checkpoints (SAC) which in turn compromised meiotic maturation in mouse oocyte, featured by the attenuation of polar body extrusion (PBE). Detection of cytoskeletal dynamics demonstrated that CTL exposure weakened the acetylation level of alpha-tubulin and impaired meiotic spindle apparatus, which was responsible for the aberrant state of SAC. Meanwhile, exposure to CTL damaged the function of mitochondria, inducing the decline of ATP content and the elevation of reactive oxygen species (ROS), which thereby induced early apoptosis and DNA damage in mouse oocytes. In addition, exposure to CTL caused the alteration of the level of histone H3 methylation, indicative of the harmful effects of CTL on epigenetic modifications in oocytes. Further, the CTL-induced oxidative stress activated mitogen-activated protein kinase (MAPK) pathway and injured the maturation of oocytes. In summary, exposure to CTL damaged mouse oocyte in vitro maturation via destroying spindle assembly, inducing oxidative stress and triggering MAPK pathway activation.