Guangdong Ocean University

Studying the salt tolerance mechanisms of rice under a single substrate has certain limitations. The salt tolerance strategies of rice may differ under different substrate conditions. This study established three substrate types by adjusting the proportions of laterite, peat moss, and river sand: S1 (high sand; low nutrient), S2 (medium sand; medium nutrient), and S3 (low sand; high nutrient). Compared with the respective fresh water control, the magnitude of dry weight reduction in each substrate gradually decreased (S1-S3), indicating that the salt stress was effectively alleviated. KEGG enrichment analysis of differentially expressed genes (DEGs) showed that Xiangliangyou900 may be more dependent on the remodeling of carbon metabolism pathway (compared to nitrogen metabolism) in S1, but the nitrogen metabolism pathway were more significant in S3. In S3, differential metabolites were significantly enriched in carbon and nitrogen metabolism pathways, but no such enrichment was found in S1, indicating that the S3 substrate, with its high nutrient and low river sand content, is more likely to trigger carbon and nitrogen metabolism remodeling. Under salt stress, the methylation level of C bases in the CHH type increased in S1 and decreased in S3. The methylation level of CHH-type C bases in the whole genome was more strongly correlated with the physicochemical parameters of the substrate (compared to CG and CHG types).This study speculated that rice may optimize its ability to adapt to salt stress by specifically regulating the methylation of CHH-type C bases to mediate gene expression. The results of this study help enrich the theoretical system of the rice salt stress response mechanism.

The global rise of antimicrobial resistance has intensified the demand for novel antimicrobial agents with broad-spectrum efficacy and unique mechanisms of action. Herein, a marine-derived strain, Bacillus velezensis (B. velezensis) AM12, exhibiting clear inhibitory activity against eight major foodborne pathogens, was isolated from coastal seawater near Zhanjiang, China. Whole-genome sequencing revealed a 3,992,266 bp circular chromosome with a GC content of 46%, and functional annotation indicated extensive metabolic potential. Genome mining using the antiSMASH platform identified 14 secondary metabolite biosynthetic gene clusters, including those encoding surfactin, macrolactin H, bacillaene, fengycin, difficidin, bacillibactin, and bacilysin, as well as several additional clusters potentially responsible for the biosynthesis of novel antimicrobial compounds. Analysis using the BAGEL4 database further detected four bacteriocin/RiPP biosynthetic loci, corresponding to Competence/ComX, Amylocyclicin, LCI, and a Lichenicidin-like cluster. These collectively explain the broad-spectrum antibacterial activity of AM12 and suggest potential antifungal capability. Notably, the core genes of ComX and LCI exhibited relatively low similarity (46.67% and 73.91%, respectively) to known references, and B. velezensis AM12-origin lichenicidin component 2 showed no detectable homology, suggesting that AM12 may encode structurally and functionally distinct novel bacteriocins. Comparative genomic analysis with closely related terrestrial B. velezensis strains revealed that AM12-specific genes are predominantly enriched in functions associated with marine environmental adaptation and antimicrobial activity. Furthermore, machine learning-based prediction using the AM12-specific gene set identified seven high-confidence antimicrobial peptide candidates characterized by cationic charge, amphipathicity, and structural stability. This study elucidates the genomic and molecular basis of the broad-spectrum antibacterial activity pertaining to B. velezensis AM12, and establishes a systematic framework for the identification of novel antimicrobial peptides, offering candidate genes for subsequent functional characterization.

Heat stress (HS) is a significant challenge in broilers, which has a negative impact on liver health and metabolic function, endangering broiler production. This study aimed to evaluate the protective effects of dietary fucoidan (FUC) in mitigating HS-induced liver injury and to elucidate the underlying mechanisms. A total of 240 male Arbor Acres (AA) broilers at 21 days of age were randomly divided into five groups: thermoneutral (TN) group, HS group, and HS group supplemented with 200, 400, or 800 mg/kg FUC, respectively. Based on comprehensive assessments of liver histopathology, liver index, and serum biochemical markers-related to liver function (TP, ALB, AST, ALT), 800 mg/kg FUC was identified as the effective dose for alleviating HS-induced hepatic injury, resulting in improvements in liver architecture and function. Further investigations revealed that 800 mg/kg FUC enhanced hepatic antioxidant capacity by increasing T-AOC, T-SOD, and GSH-Px activities in broilers under HS. The non-targeted metabolomics analysis suggested that FUC improves six metabolites in the liver of broilers subjected to HS, including Glu-Asp-Gln, Asn-Pro-Tyr, Glu-Thr-Ile, N-Acetylleucylalanylserine, Octadecyl Fumarate, and Oleoyl-l-Carnitine. The differential metabolites were significantly enriched in several metabolic pathways, such as glycerophospholipid metabolism, fatty acid degradation, and ferroptosis. Furthermore, dietary FUC enhanced the expression of antioxidant genes (GCLC, GCLM, HO-1, SOD2, GPX1, GPX3, CAT1, and GSTA3), suppressed lipogenic genes (SREBP-1, FAS, and ACC), and upregulated the lipolytic gene ATGL as well as the adipogenic regulator PPARγ in the liver of broilers under HS. Additionally, FUC downregulated pro-ferroptotic genes (ACSL4, LPCAT3, and PTGS2) while upregulated anti-ferroptotic genes (Fpn1, FTH1 and SLC7A11) in the liver of heat-stressed broilers. Western blot analysis confirmed that FUC activated the Nrf2 signaling pathway by increasing the protein expression of Nrf2, phosphorylated Nrf2 (p-Nrf2), and nuclear p-Nrf2, while upregulated the AMPK pathway by increasing AMPK and phosphorylated AMPK (p-AMPK) protein levels of the liver in broilers subjected to HS. These findings indicate that dietary supplementation with 800 mg/kg FUC ameliorates HS-induced liver injury through the activation of Nrf2-mediated antioxidant and anti-ferroptosis signaling, and the regulation of AMPK-mediated lipid metabolism balance. This study provides a dietary strategy to improve liver health in heat-stressed broilers, which is beneficial for broiler production during the hot season.