Intercropping is emerging as a sustainable strategy for managing soil-borne diseases; however, its underlying mechanisms remain largely unknown. In this study, we used 16S rRNA sequencing, ITS amplicon sequencing, and untargeted metabolomics to investigate the mechanisms through which soybean intercropping (DS) affects root rot disease incidence. The results revealed that intercropping significantly increased the survival rate of tobacco plants under Fusarium spp. infection (P < 0.01). DS increased soil microbial community diversity and significantly reduced the relative abundance of Fusarium (by 53.17%). At the genus level, Fusarium (LDA = 4.34) was significantly enriched in DT (Tobacco monoculture soil). In contrast, the DS treatment led to significant enrichment of Peziza (LDA = 5.17) and Mortierella (LDA = 4.25). DS increased the complexity of the microbial association network, as evidenced by a 49.23% increase in nodes and a 79.2% increase in edges. However, the complexity of the Fusarium subnetwork decreased, as evidenced by a 50.00% reduction in nodes and an 83.33% reduction in edges. These shifts are attributed primarily to alterations in the differential microbial communities. Metabolomic analysis revealed that DS promoted the accumulation of indole (log2FC = 3.79, VIP = 2.09), and the indole content was significantly negatively correlated with Fusarium abundance. The plate assay results demonstrated that the inhibitory effect of indole on Fusarium colony growth increased with concentration, with an inhibition rate of 37.71% observed at 800 μM indole. In conclusion, this study provides a theoretical basis for leveraging intercropping to modulate the rhizosphere microenvironment and control soil-borne diseases, thereby meriting regional-scale pilot promotion.

Galeruca daurica (Joannis) (Coleoptera: Chrysomelidae) is an oligophagous pest in which both adults and larvae prefer to feed on Allium forage grasses of the Liliaceae family. In this study, we identified gustatory receptor (GR) genes based on the transcriptome data of G. daurica; analyzed the expression profiles of these GR genes across different larval instars and various tissues of male and female adults using quantitative real-time PCR (qRT-PCR); detected the electrophysiological responses of the mouthparts of male and female G. daurica adults to flavonoids and carbohydrates using single sensillum recording (SSR); and recorded the changes in food consumption of G. daurica adults after feeding on six host plant-derived metabolites. A total of 26 GR genes were identified from the transcriptome data of adult and larval of G. daurica. Phylogenetic analysis was performed to screen candidate functional gustatory receptor genes, including four sugar receptors (GdauGR7, GdauGR10, GdauGR14 and GdauGR28), seven bitter receptors (GdauGR11, GdauGR16~17, GdauGR22, GdauGR25~26 and GdauGR30), and two CO2 receptors (GdauGR15 and GdauGR20). Larval expression profiling of GdauGRs in G. daurica revealed that the relative expression levels of 17 genes exhibited dynamic changes during larval growth and development. GdauGRs were expressed to varying degrees in the antennae, mouthparts, brain, gut, and forelegs of adult G. daurica, with sex-specific differences. Notably, the expression levels of GdauGR4, GdauGR9 and GdauGR16 in the gut were extremely significantly higher than those in other tissues. In the SSR test, the six tested flavonoids and one carbohydrate were able to induce robust electrophysiological responses in the gustatory sensilla on the antennae and mouthparts of adult G. daurica at specific concentrations. In addition, the supplementation of several host-derived metabolites altered the food consumption of adult G. daurica. These findings lay a solid foundation for elucidating the molecular mechanisms underlying gustatory recognition and host adaptation in G. daurica.

The differential fat deposition in intramuscular (IMF) and subcutaneous (SCF) adipose tissues significantly influences goat meat quality. While microRNAs (miRNAs) are key post-transcriptional regulators, the shared key miRNAs governing adipogenesis across different adipose depots remain largely unexplored in goats. In this study, intramuscular and subcutaneous preadipocytes were isolated from the same healthy 7-day-old male Jianzhou Da'er goat, and each experimental group comprised five independently cultured cell replicates derived from this donor. Integrated miRNA and mRNA sequencing was performed on undifferentiated intramuscular (JNE) and subcutaneous (PE) preadipocytes and their corresponding adipocytes after 72 h of differentiation (JNC and PC, respectively), allowing the identification of depot-specific and shared differentially expressed miRNAs (DEmiRNAs) and mRNAs (DEmRNAs). By constructing miRNA-mRNA regulatory networks, chi-miR-1 was identified as the highest-degree miRNA node in the shared network and was therefore prioritized for functional evaluation. RT-qPCR, chi-miR-1 mimic and inhibitor transfection, Oil Red O staining, and BODIPY staining showed that chi-miR-1 overexpression increased lipid droplet accumulation, whereas its inhibition produced the opposite effect in both intramuscular and subcutaneous adipocytes. Furthermore, bioinformatic target prediction and network analysis identified chi-miR-1-PPARG and chi-miR-206-IGFBP3 as predicted potential regulatory relationships; these interactions were not directly validated experimentally. Our findings, obtained using cells derived from a single donor, suggest that chi-miR-1 may serve as a candidate shared pro-adipogenic regulator under the present in vitro conditions and provide insights into miRNA-mediated regulation of adipogenesis in different goat adipose depots.

Intramuscular fat (IMF) is a key meat quality determinant. While coated methionine (CM), 2-hydroxy-4-(methylthio)-butanoic acid (HMBA) and its isopropyl ester (HMBi) enhance milk fat in dairy cows, their effects on IMF in meat ruminants remain unclear. A total of 30 goats (n = 10 per treatment) were assigned to basal diet, or basal diet plus 0.12% CM or 0.22% HMBi for a 4.5-month feeding trial. Carcass traits, meat quality and serum lipid profiles were determined. Results showed HMBi increased live and carcass weights, while both CM and HMBi reduced GR value, shear force and moisture content. HMBi increased IMF, total, saturated and monounsaturated fatty acids, while CM increased most amino acids in Longissimus thoracis et lumborum (LTL) muscle. Furthermore, HMBi upregulated adipogenic genes and downregulated lipolytic genes, whereas CM downregulated both in LTL muscle. Both CM and HMBi significantly increased serum APOA1 and decreased TG/HDL-C, while HMBi alone also increased HDL-C and decreased LDL-C. In vitro experiments showed HMBA had a quadratic relationship with intramuscular preadipocyte proliferation and differentiation (max at 200 μM). Transcriptomics revealed it altered immune/inflammatory/apoptotic pathways and promoted fat deposition via APOH inhibition. Collectively, HMBi outperformed CM in growth promotion. HMBi enhanced IMF deposition via APOH downregulation, while CM promoted amino acid accumulation, laying a foundation for methionine use in meat quality improvement in meat ruminant.

Tobacco root rot (TRR), caused by Fusarium oxysporum, poses a significant threat to tobacco production. Synthetic fungicides widely used to control this soil-borne pathogen frequently cause fungicide resistance and environmental contamination. Limonene, a natural terpene with potent antifungal activity, features low residue and high biosafety, rendering it a promising natural substitute for chemical fungicides against TRR. This study aimed to investigate the antifungal activity and mechanisms of limonene against F. oxysporum using in vitro assays, physiological tests, transcriptomics, and metabolomics. The results demonstrated that limonene significantly inhibited mycelial growth and spore proliferation, with an EC50 of 201.2 μg/mL (1.48 mM). It exhibited a dose-dependent repellent effect on the chemotactic behavior of F. oxysporum, with effective concentrations as low as 25 μg/mL (0.18 mM). Furthermore, it disrupted cell membrane integrity and permeability at concentrations as low as 100 μg/mL (0.73 mM). Transcriptomic screening identified 3,871 differentially expressed genes (DEGs), which were significantly enriched in ribosome, proteasome, ER protein processing, autophagy and glyoxylate metabolism pathways. Eight representative key DEGs (cat1, rhogap, tf, cyc, bro1, mic12, rpl13, clptm1l) related to fungal growth and stress response were verified by RT-qPCR verification, and their expression trends were consistent with the transcriptomic results. Metabolomic analysis revealed 626 differential accumulated metabolites (DAMs), three key metabolites (ortho-Hydroxyphenylacetic acid, 4-Methylphenol and Lenticin) were significantly altered under limonene treatment. These DAMs were mainly enriched in starch and sucrose, riboflavin, folate and tyrosine metabolism pathways. Multi-omics joint analysis indicated that key targeted pathways including energy metabolism, amino acid metabolism, lipid metabolism, and protein synthesis and degradation were regulated. In conclusion, limonene inhibits F. oxysporum through multiple mechanisms, including cell membrane damage, chemotaxis blockage, transcriptional regulation, and metabolic disturbance. This study provides scientific support for the development of limonene as a green botanical fungicide for controlling tobacco root rot.

BACKGROUND:20-hydroxyecdysone (20E) coordinates insect reproductive development through extensive metabolic reprogramming. However, the post-transcriptional mechanisms linking hormonal signaling to carbohydrate metabolism during reproductive maturation remain poorly understood in insect pests. RESULTS:We identified a novel 20E-miR-2788-Treh1 regulatory axis in Galeruca daurica. Developmental profiling revealed an inverse relationship between miR-2788 and Treh1 expression. Overexpression of miR-2788 or RNA interference (RNAi)-mediated silencing of Treh1 caused trehalose accumulation, reduced expression of chitin biosynthesis genes, and impaired ovarian development. In females, 20E treatment suppressed miR-2788 expression and increased Treh1 expression, thereby promoting ovarian maturation. Similar reproductive defects were induced by the trehalase inhibitor validamycin. CONCLUSION:These findings suggest that 20E- reproductive miR-2788-Treh1 module contributes, at least in part, to the regulation of reproductive maturation through the -mediate control of trehalose metabolism. The 20E-miR-2788-Treh1 axis represents an important metabolic checkpoint linking endocrine signaling with reproductive development and provides potential molecular targets for environmentally friendly pest management strategies. © 2026 Society of Chemical Industry.

Tobacco Fusarium wilt (TFW), caused by Fusarium spp., is a destructive disease affecting tobacco crops and resulting in significant economic losses. The current chemical fungicide-based management strategy poses a risk of resistance development in pathogens. In order to identify key factors in the tobacco rhizosphere for sustainable TFW control, untargeted metabolomics and microbiomics were conducted to analyze the key metabolites and microbes between healthy and diseased rhizosphere soils. The results revealed a total of 65 differential metabolites (DMs), with 40 upregulated and 25 downregulated were identified in the diseased group. Among these, Aesculin, 8-Deoxy-11-hydroxy-13-chlorogrosheimin, and N-Gluconyl ethanolamine phosphate were identified as key DMs exhibiting a strong negative correlation with healthy soil status. The microbiome analysis revealed that bacterial diversity (OTUs: 3278 vs. 3039; Shannon: 6.72 vs. 6.65) and fungal diversity (OTUs: 919 vs. 701; Shannon: 3.91 vs. 3.44) were significantly higher in healthy soils. Furthermore, co-occurrence networks in healthy soils were larger and more stable, with bacteria comprising 431 nodes compared to 405 in diseased soils, and fungi comprising 112 nodes compared to 101 in diseased soils. Additionally, the analysis of the microbial community assembly process revealed that deterministic processes dominated microbial assembly in healthy soils during the first 75 d, subsequently shifting toward stochastic processes. In contrast, diseased soils exhibited a consistently deterministic assembly. Furthermore, we observed that variations in soil types influenced the distribution of key microbial groups. Chloroflexi, Bryobacter, Bacillus, Preussia, and Tausonia, were enriched in healthy soils while Lysobacter, Arthrobacter, Fusarium, and Lectera were dominated in diseased soils. The combined analysis results indicated that the three key DMs correlated positively with disease-enriched microbes but negatively with health-associated taxa. This study provides insights into the changes in and microbe-metabolite interactions within the tobacco rhizosphere under pathogen stress and supports the future development of TFW control strategies based on key metabolites and microbes.

Metamorphosis in insects is regulated by hormonal signals and metabolic pathways. In this study, we characterized a 20E-mediated miR-2788/Treh1 regulatory axis involved in the larval-to-pupal transition in the leaf beetle Galeruca daurica. Dual-luciferase assays and expression profiling suggest that miR-2788 directly targets and suppresses trehalase 1 (Treh1), a key enzyme for trehalose hydrolysis. We found that exogenous 20E treatment significantly downregulated miR-2788, leading to the derepression of Treh1 and increased expression of chitin biosynthetic genes (CHI, CHS, and GPI). Conversely, miR-2788 overexpression or Treh1 silencing via RNAi resulted in massive trehalose accumulation, reduced chitin synthesis, and lethal developmental arrest during the metamorphic transition. Furthermore, pharmacological inhibition of Treh1 with Validamycin not only recapitulated these chitin-deficiency phenotypes but was also associated with an upregulation of miR-2788. These results describe a signaling cascade where 20E modulates the conversion of carbohydrate to chitin through the miR-2788/Treh1 axis. This study advances our understanding of hormonal-miRNA-metabolic crosstalk and identifies miR-2788 as a potential target for RNAi-based biopesticide development.

Tobacco root rot (TRR) caused by Fusarium oxysporum severely restricts sustainable tobacco production worldwide. In this study, endophytic bacteria were isolated from healthy tobacco plants collected from continuously cropped fields, and a dominant antagonistic strain, NRM3001, was identified as Alcaligenes faecalis based on morphological, physiological, biochemical, and 16S rRNA analyses. Strain NRM3001 exhibited strong broad-spectrum antagonistic activity against multiple tobacco pathogens, with inhibition rates of 96.00% against F. oxysporum, 95.20% against Phytophthora nicotianae, and 98.50% against Alternaria alternata. The strain also possessed phosphate-solubilizing ability, siderophore production capacity, and significant growth-promoting effects on tobacco seedlings. Pot experiments demonstrated that preventive application of NRM3001 effectively reduced TRR incidence, with a relative control efficacy of 80.85%. Transcriptome analysis revealed that NRM3001 significantly suppressed genes involved in oxidative phosphorylation, the tricarboxylic acid cycle, and ribosome biogenesis pathways in F. oxysporum, thereby disrupting fungal energy metabolism and protein synthesis. In addition, fermentation conditions optimized via Plackett–Burman design and response surface methodology (RSM) yielded a 43.2% increase in bacterial biomass. Field trials further confirmed the stable biocontrol effect of NRM3001 against TRR in naturally diseased fields, with a relative control efficacy of 73.18%. These findings indicate that A. faecalis NRM3001 is a promising biocontrol agent for the sustainable management of TRR in tobacco, an important industrial non-food crop.

Hematopoietic stem cell transplantation (HSCT) is a cornerstone treatment for blood disorders and hematological malignancies, although its efficacy is limited by inefficient stem cell homing to the bone marrow. We previously demonstrated that fucosylated HSC ligands interact with endothelial E-selectin to facilitate homing. However, the downstream consequences of modulating fucosylation in HSCs remain unclear. Here, we systematically characterized how enhancing or inhibiting fucosylation—via recombinant human fucosyltransferase 6 (FTVI) or 2-fluoro-L-fucose (2FF), respectively—affects migration, signaling, and engraftment of human granulocyte-colony stimulating factor-mobilized peripheral blood CD34⁺ (mPB-CD34⁺) cells. Live-cell imaging under flow, phosphoproteomics, and transcriptomics were used to characterize rolling dynamics and intracellular signaling, and in vivo homing was assessed in immunodeficient xenograft mouse models. Fucosylation enhanced tether and sling formation, improved E-selectin binding, and increased homing to the bone marrow and spleen. FTVI-treated cells activated MAPK and PI3K/AKT/mTOR pathways and showed enriched Rho-GTPase signaling, associated with proliferation and migration. In contrast, 2FF-treated cells had impaired migration and reduced rolling efficiency. Long-term xenograft studies showed enhanced bone marrow engraftment/persistence of fucosylated cells without altering lineage output. Fucosylation critically modulates E-selectin interactions, migration, and intracellular signaling in HSCs. These findings highlight glycoengineering as a promising strategy to enhance HSC transplantation outcomes in cancer therapy.

GPR35 is a member of the G-protein-coupled receptor family and existing studies have shown that its expression may be negatively correlated with fat deposition in mice. However, the exact role of GPR35 in goat intramuscular preadipocytes’ adipogenic differentiation remains unknown. This study is the first to demonstrate that GPR35 inhibits the maturation and differentiation of goat intramuscular preadipocytes via activating the cAMP/PKA signaling pathway under in vitro culture conditions. The functional experimental results showed that GPR35 overexpression suppressed the adipogenic differentiation, lipid synthesis, and proliferation capacity of goat intramuscular preadipocytes, and concurrently downregulated the expression of adipogenic differentiation marker genes and cell proliferation marker genes. Conversely, GPR35 knockdown promoted lipid accumulation, reduced intracellular cAMP levels, and ultimately enhanced the differentiation and proliferation capacity of intramuscular preadipocytes. Treatment with the cAMP inhibitor SQ22536 and PKA phosphorylation inhibitor H89 successfully reversed the phenotypic changes induced by GPR35 overexpression, including abnormal lipid droplet morphology, decreased triglyceride (TG) content, and inhibition of the expression of genes related to adipocyte differentiation/proliferation/metabolism (such as CDK2, PCNA, and HSL). These results confirm that GPR35 mainly regulates intramuscular fat deposition in goats through the cAMP/PKA pathway, providing a new target for elucidating the molecular mechanism of lipid metabolism and goat molecular breeding.

Background Galeruca daurica (Joannis), a notorious pest in Northern China, seriously threatens Inner Mongolia grassland ecosystems and economy, due to its strong cold hardiness and huge outbreak in a short time. Despite previous studies emphasized molecular mechanisms in response to low-temperature stress, especially based on studies of key gene functions on cold hardiness, there is a lack of in-depth research on transcriptional regulation mechanisms. Results The G . daurica eggs, collected from the grassland of Xianghuang Banner of Xilin Gol League in Inner Mongolia, were reared to the 1st and 2nd instar larvae at different temperatures. RNA-Seq analyzed differentially expressed genes (DEGs) in larvae reared in different states. Weighted gene co-expression network analysis (WGCNA) identified cold hardiness-related gene modules, and regulatory network analyses screened key transcription factors (TFs). The Gene Transcription Regulation Database (GTRD) predicted HSF1 target genes. The genes of HSF1 , HSP26 , and HSP68 were knocked down to evaluate the impacts on expression and cold hardiness. The blue module showed the highest cold hardiness correlation, with HSF1 as a key regulator. Silencing HSF1 decreased HSP26 and HSP68 expression, and knocking down these HSPs reduced the expression of HSF1 . Silencing HSF1 , HSP28 , and HSP86 can increase super-cooling points (SCPs) and freezing points (FPs) significantly. HSF1 regulates HSP26 and HSP68 expression to enhance the cold hardiness of G. daurica . These results elucidate the molecular mechanisms underlying cold hardiness and provide new insights into the adaptability of insects to extreme environments. Conclusions The RNA-Seq analysis of G. daurica has revealed a potential regulatory relationship among HSF1 , HSP26 , and HSP68 . The increased SCPs and FPs after RNAi support their roles in low-temperature tolerance. These findings provide preliminary insights into the molecular basis of cold hardiness in G. daurica.

The aim of this study was to detect the expression of GSK3B gene in different tissues of goats and the expression level of intramuscular precursor adipocytes at different differentiation periods, and to further reveal the effects of overexpression and interferences of GSK3B gene on lipid deposition in intramuscular precursor adipocytes of goats. The results showed that a nucleotide sequence of 1,433 bp, CDS region 1,263 bp, encoding 420 amino acids, was obtained for the goat GSK3B gene, Goat GSK3B gene expression was highest in the lungs, lowest in the longest dorsal muscle, and highest at 120 h of induced differentiation. Overexpression of GSK3B gene significantly reduced lipid droplets in intramuscular precursor adipocytes, and also significantly down-regulated the relative expression of SREBP1, CEBP beta and PPAR gamma (p < 0.05), with no significant changes in the expression of FASN, CEBP alpha, SCD and LPL (p > 0.05), GSK3B inhibition increased lipid droplets accumulation by significantly down-regulated SREBP1, CEBP beta and PPAR gamma expression (p < 0.05). In conclusion, GSK3B expression significantly inhibited lipid deposition in goat intramuscular precursor adipocytes. These results provide important data to further elucidate the molecular mechanisms regulating intramuscular fat formation in goats.

Background:The development of metabolic dysfunction-associated steatotic liver disease (MASLD) is closely associated with cardiovascular health (CVH) status and chronic inflammation. Life's Crucial 9 (LC9) is the most recent index to assess CVH; its association with MASLD and liver fibrosis is unclear. This study aimed to investigate the association of LC9 with MASLD and hepatic fibrosis and to reveal for the first time the mediating role of a novel inflammatory marker, neutrophil percentage-to-albumin ratio (NPAR), in the association between LC9 and MASLD. Methods:This study was a cross-sectional analysis of data from the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018. The United States Fatty Liver Index (US-FLI) ≥ 30 was used to diagnose MASLD, and liver stiffness measurement (LSM) > 8.2 is defined as liver fibrosis. Weighted multifactorial regression, restricted cubic spline analysis (RCS), and subgroup analyses were used to assess the association between LC9 and MASLD and liver fibrosis. Mediation analysis was used to explore the possible mediating role of NPAR in the association of LC9 with MASLD. Results:A total of 9,623 participants were included in this study. After adjusting for all confounders, LC9 was significantly and negatively associated with both MASLD (OR = 0.59, 95% CI: 0.54-0.64) and hepatic fibrosis (OR = 0.66, 95% CI: 0.45-0.97), with each 10-point increase in the LC9 score decreasing the prevalence by 41% and 34%, respectively. In subgroup analyses, interaction tests showed that age, education, deprivation, obesity, smoking, hypertension, diabetes, and hyperlipidemia significantly affected the association between LC9 and MASLD (P for interaction < 0.05). In addition, NPAR was positively associated with the prevalence of MASLD, with a 5% increase in the prevalence of MASLD for each unit increase in NPAR (OR = 1.05, 95% CI: 1.01-1.09). The positive association between NPAR and MASLD was stronger in younger age groups (<60 years), non-drinkers, and participants without diabetes or hyperlipidemia. Mediation analysis showed that NPAR mediated 2.84% of the association between LC9 and MASLD (p < 0.001). Conclusion:Good CVH status (high LC9 score) was associated with lower prevalence of MASLD and liver fibrosis, and NPAR partially mediated the association between LC9 and MASLD. This study provides new epidemiological evidence for preventing MASLD by improving CVH and inflammatory modulation.

Plants perceive microbe-derived molecular patterns to initiate the innate immune system. The csp22 peptide, derived from bacterial cold shock protein, is uniquely recognized by cold shock protein receptor (CORE) in Solanaceae plants, yet the signaling pathway remains largely obscure. In this study, we identify that tomato csp22-activated kinase 1 (SlCAK1), belonging to the receptor-like cytoplasmic kinase subgroup VII, is essential for csp22-induced immune responses and resistance to bacterial wilt disease. SlCAK1 is rapidly recruited to the csp22 receptor complex, which results in SlCAK1 phosphorylation upon csp22 treatment. Notably, csp22-induced phosphorylation specifically occurs at the Ser60 residue in the N terminus of SlCAK1, which is critical for SlCAK1 function in immunity. Interestingly, the conservation of Ser60 is unique to Solanaceae plants. Taken together, our findings reveal the pivotal role of SlCAK1 in transducing csp22-triggered immune signaling and provide a novel activation mechanism for receptor-like cytoplasmic kinases that involves phosphorylation in the N terminus.

Vitamin A (VA) and its active form, retinoic acid (RA), are crucial for preserving hepatic stellate cells (HSCs) quiescence and reversing fibrosis. While C6orf120 is known to be involved in HSC activation, its role in RA signaling is unclear. This study found that C6orf120 knockdown markedly reduced CCL4-induced liver fibrosis and TGF-β1-induced activation in LX-2 cells, a human HSC line. This inhibition was associated with enhanced RA signaling, particularly affecting the RA receptor beta (RARβ). Inhibition of RARβ significantly reversed the protective effects of C6orf120 knockdown, indicating that RARβ signaling contributes to the inhibitory effect of C6orf120 knockdown on HSC activation. Our results reveal that C6orf120 inhibition could be a therapeutic strategy for liver fibrosis by regulating RARβ signaling.

Hematopoietic stem cell transplantation (HSCT) efficacy is often limited by inefficient stem cell delivery to the bone marrow and challenges in maintaining transplanted hematopoietic stem cell (HSC) pools. We investigated the impact of modulating α1,3-fucosylation on human peripheral blood CD34+ HSCs, a modification known to improve E-selectin binding through sialyl Lewis X (sLex) expression. Our findings demonstrate that fucosylation-enhanced HSCs exhibit improved rolling by forming elongated tethers and slings, leading to stronger adhesion to E-selectin. This enhanced adhesion facilitated increased homing and engraftment of fucosylated HSCs in the bone marrow and spleen of immunocompromised mice, while inhibiting fucosylation with 2-Fluoro-fucose (2FF) significantly impaired these processes.Further, phosphoproteomic and transcriptomic analyses revealed that enhanced E-selectin binding in fucosylated cells activates key intracellular signaling pathways. Notably, Rho-GTPases, associated with migration and adhesion, and EGFR/PI3K/AKT/mTOR and MAPK pathways, linked to cell cycling, were stimulated. We observed that fucosylation stimulates cell cycling, boosting self-renewal and engraftment, while also enhancing HSC adhesion, quiescence, and marrow retention. These changes appear to preserve long-term stemness, suggesting a multifaceted role for fucosylation in regulating both short-term engraftment and durable hematopoietic reconstitution. This study provides a comprehensive mechanistic understanding of how fucosylation impacts HSC function, highlighting its potential as a powerful strategy to improve HSCT outcomes by optimizing stem cell delivery, engraftment, and long-term hematopoietic reconstitution

Adipose tissue affects not only the meat quality of domestic animals, but also human health. Adipocyte differentiation is regulated by a series of regulatory genes and cyclins. Four and half-LIM protein (FHL2) is positively correlated with the hypertrophy of adipocytes and can cause symptoms such as obesity and diabetes. In the transcriptome sequencing analysis of intramuscular adipocytes after three days of differentiation, the differentially expressed gene FHL2 was found. To further explore the biological significance of the differentially expressed gene FHL2, which was downregulated in the mature adipocytes. We revealed the function of FHL2 in adipogenesis through the acquisition and loss of function of FHL2. The results showed that the overexpression of FHL2 significantly increased the expression of adipogenic genes (PPARγ, C/EBPβ) and the differentiation of intramuscular and subcutaneous adipocytes. However, silencing FHL2 significantly inhibited adipocyte differentiation. The overexpression of FHL2 increased the number of adipocytes stained with crystal violet and increased the mRNA expression of proliferation marker genes such as CCNE, PCNA, CCND and CDK2. In addition, it significantly increased the rate of EdU positive cells. In terms of apoptosis, overexpression of FHL2 significantly inhibited the expression of P53 and BAX in both intramuscular and subcutaneous adipocytes, which are involved in cell apoptosis. However, overexpression of FHL2 promoted the expression of BCL, but was rescued by the silencing of FHL2. In summary, FHL2 may be a positive regulator of intramuscular and subcutaneous adipocyte differentiation and proliferation, and acts as a negative regulator of intramuscular and subcutaneous adipocyte apoptosis. These findings provide a theoretical basis for the subsequent elucidation of FHL2 in adipocytes.