Search Results (6,990)

Hair follicles are highly specialized mini-organs within the skin that drive the production of wool and cashmere, traits of major biological and economic importance in sheep and goats. Despite their microscopic size, hair follicles exhibit extraordinary regulatory complexity, integrating genetic programs with seasonal, endocrine, environmental, and epigenetic cues. Although transcriptional networks and signaling pathways underlying follicle morphogenesis and cycling have been extensively investigated, the post-transcriptional mechanisms that fine-tune these processes remain insufficiently understood. MicroRNAs (miRNAs) have emerged as pivotal post-transcriptional regulators that coordinate cell fate determination, lineage commitment, and tissue homeostasis. Growing evidence indicates that miRNAs play essential roles in hair follicle stem cell maintenance, proliferation, differentiation, apoptosis, and organ-level development, functioning through interconnected regulatory networks rather than isolated linear pathways. By modulating the expression of key follicle-determining genes and signaling components, miRNA-mediated regulation shapes follicle formation, cyclic regeneration, and fiber traits. In this review, we synthesize recent advances in miRNA research related to hair follicle biology, with a particular focus on wool- and cashmere-bearing mammals. We integrate findings across species to propose a systems-level framework in which miRNA networks interface with canonical signaling pathways and epigenetic mechanisms to orchestrate follicle development and regeneration. Conserved and species-specific regulatory principles are discussed to bridge fundamental follicle biology with practical applications in fiber production. Overall, this review highlights miRNAs as a critical yet previously underappreciated regulatory layer in hair follicle biology. A deeper understanding of miRNA-mediated control provides new conceptual insights into wool and cashmere development and offers a foundation for future molecular breeding and precision regulation strategies in livestock. Full article

Premium coffee depends on high-quality beans, influenced by a combination of genetic, environmental, and postharvest factors. This review summarizes the mechanisms underlying coffee bean quality, with an emphasis on the genetic differences between Coffea arabica and Coffea canephora, as well as the integrated roles of environmental conditions, agronomic practices, including nutrient and shade management, and postharvest processing technologies. The allotetraploid genome of C. arabica is influenced by homoeologous exchanges and subgenome-biased expression (such as decreased DXMT activity that reduces caffeine), which contribute to its complex flavor profile. Key lipid metabolism genes, particularly FADS2, play a critical role in regulating lipid metabolism. The effects of altitude (1600–2000 m) and shade influence various metabolic pathways. Cooler temperatures promote sugar accumulation, while excessive shading hinders carbon assimilation and the development of flavor precursors. Postharvest processing significantly influences flavor, where microbial or enzymatic treatments enhance sensory attributes. In addition, methods like natural, washed, or honey processing modulate various nonvolatile compounds, impacting lipid emulsification and aroma retention. Multi-omics analyses suggest that MYB proteins play a key role in regulating pathways involved in caffeine, chlorogenic acids, and terpenes. Effective hermetic packaging prevents oxidation, thereby preserving freshness. Overall, superior coffee quality stems from synergistic interactions across genetic, ecological, agronomic, and processing factors, highlighting the need for the development of an integrated strategy to support the sustainable production of premium coffee. Full article

Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing post-irradiation BM injury remain incompletely defined. Methods: This study aimed to systematically identify radiation-responsive pathways and central genes in BM after irradiation through an integrative bioinformatics approach based on RNA sequencing (RNA-seq). Public RNA-seq data from mouse BM HSCs collected 3 days after whole-body irradiation were analyzed. Differentially expressed genes (DEGs) were identified using two independent statistical frameworks to improve the robustness of the results. Functional analysis was performed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Protein–protein interaction (PPI) networks were constructed using STRING, and hub genes were identified using network topology parameters. Results: Both analysis pathways consistently demonstrated extensive transcriptome reprogramming after irradiation. DEGs were primarily enriched in processes related to cytokine signaling, hematopoietic lineage regulation, immune response, and extracellular matrix remodeling. KEGG analysis highlighted cytokine–cytokine receptor interaction, hematopoietic cell lineage, JAK-STAT signaling, and PI3K-Akt signaling as key molecular axes. GSEA further supported coordinated changes in pathways related to inflammatory response, stress response, and metabolic reprogramming. PPI network analysis identified four consensus hub genes, namely Il6, Cd34, Gypa, and Pdgfrb, which are related to inflammatory signaling, hematopoietic regulation, erythroid dynamics, and microenvironmental remodeling, respectively. Conclusion: This integrative bioinformatics study demonstrates that radiation-induced BM injury is associated with coordinated activation of inflammatory cytokine networks, alterations in the hematopoietic program, and microenvironmental restructuring. The hub genes identified in this study may represent candidate regulatory genes or molecular indicators potentially involved in the response to radiation-induced hematopoietic damage. Full article

Background: Infections caused by multidrug-resistant bacteria and inadequate vaccine coverage against opportunistic pathogens highlight the need for interventions that broadly and durably enhance host defense beyond antigen-specific adaptive immunity. Trained immunity, driven by metabolic and epigenetic reprogramming of innate immune cells, has been predominantly characterized using Bacille Calmette–Guérin and β-glucan, whereas its induction by Gram-negative bacteria remains poorly defined. To address this gap, we aimed to determine whether heat-killed Klebsiella pneumoniae (HK Kp) induces trained immunity through metabolic and hematopoietic reprogramming to confer heterologous antibacterial protection. Methods: HK Kp-trained murine bone marrow-derived macrophages and HK Kp-immunized C57BL/6 mice were employed to interrogate functional, metabolic, and transcriptomic reprogramming in vitro, hematopoietic progenitor remodeling in vivo, and protective efficacy against systemic Salmonella Typhimurium and Staphylococcus aureus infection. Results: HK Kp-trained macrophages showed markedly enhanced IL-1β secretion across all restimulation conditions, stimulus-dependent amplification of TNF-α responses, increased phagocytosis, and improved intracellular control of S. typhimurium, together with sustained upregulation of the glycolytic enzymes-encoding genes Hk2 and Pfkfb3. Transcriptomic profiling revealed extensive reprogramming enriched in glycolysis/gluconeogenesis and hematopoietic cell lineage pathways. In vivo, HK Kp immunization shifted bone marrow stem/progenitor compartments toward a myeloid-biased state. HK Kp-trained mice challenged with lethal S. typhimurium or S. aureus exhibited less weight loss, improved survival rates, and reduced bacterial burdens. Conclusions: Inactivated K. pneumoniae orchestrates metabolic and hematopoietic reprogramming to establish enhanced innate immune responsiveness and confer heterologous protection in murine S. typhimurium and S. aureus sepsis models, supporting its potential as a potent inducer of trained immunity. These findings establish HK Kp-based trained immunity as a promising strategy for combating multidrug-resistant and vaccine-evading pathogens. Full article

Soil salinization has become a major global constraint threatening ecosystem stability and agricultural production. As a prominent salt-tolerant turfgrass, Paspalum vaginatum (seashore paspalum) serves as an excellent material for exploring salt tolerance mechanisms. In this study, PvHAK12, a high-affinity K⁺ transporter (HAK) family gene isolated from seashore paspalum, was functionally characterized. PvHAK12 encodes a 788 amino acid protein with 13 transmembrane domains, belonging to the plasma membrane-localized ion transporters. It exhibits high sequence conservation with other HAK transporters and is predominantly expressed in roots and stems, with distinct tissue- and time-specific induction under salt stress. Yeast complementation assays revealed that PvHAK12 has no obvious K⁺ transport capacity but may mediate Na⁺ transport. Overexpression of PvHAK12 in Arabidopsis thaliana significantly reduced salt tolerance at germination, seedling and rosette stages, as reflected by lower germination rate, fresh weight, survival rate, the maximum quantum yield of photosystem II (Fv/Fm) value and chlorophyll content, accompanied by higher ion leakage. Under salt stress, transgenic plants accumulated more Na⁺ and less K⁺, leading to an elevated Na⁺/K⁺ ratio. Moreover, transgenic lines displayed weaker antioxidant enzyme activities and higher reactive oxygen species (ROS) accumulation. Transcript analysis further demonstrated that PvHAK12 overexpression suppressed the induction of multiple ion-transport and stress-responsive genes under salt conditions. These results indicate that PvHAK12 negatively regulates plant salt tolerance by disrupting ion homeostasis, antioxidant capacity and stress-related gene expression. Full article

Winter rapeseed (Brassica rapa L.) is an important crop for vegetable oil production in China. However, its productivity is frequently threatened by severe cold waves during winter. To investigate the role of the microtubule cytoskeleton in cold adaptation of winter rapeseed, a microtubule stabilizer paclitaxel (Tax) and a microtubule depolymerizer colchicine (Col) were sprayed on winter rapeseed and transgenic proBrAFP1 Arabidopsis, respectively. The mRNA levels of cold-induced genes, along with cell membrane stability, antioxidant enzyme activities, and hormone levels were assessed under cold stresses of 4 °C and −4 °C. The results showed that low temperature significantly activated the proBrAFP1 promoter activity and increased the mRNA levels of core cold signaling pathway genes, such as C-REPEAT BINDING FACTORS (CBFs), Cyclic Nucleotide-Gated Channel (CNGC), OPEN STOMATA 1 (OST1) and Inducer of CBF EXPRESSION 1 (ICE1). Notably, under low-temperature stress, exogenous application of the microtubule stabilizer Tax markedly suppressed proBrAFP1-driven reporter activity in transgenic Arabidopsis, with consistent inhibition observed across both stem and leaf tissues; meanwhile, the Tax application alleviated reactive oxygen species (ROS) accumulation and mitigated membrane damage. In contrast, under the same low-temperature stress, the Col treatment exacerbated oxidative stress, enhanced lipid peroxidation, and elevated membrane damage. Collectively, these findings establish that microtubule regulators play indispensable roles in the cold stress response of winter rapeseed. It provides new insights into the mechanism by which plant microtubule cytoskeleton regulators mediate the cold response. Full article

Pluripotent stem cell (PSC) differentiation is orchestrated by intricate autocrine and paracrine signaling networks. Among these, exosomes, key components of the cellular secretome, are implicated as crucial mediators of intercellular communication via delivery of bioactive molecules, including microRNAs (miRNAs). This study investigated the role of exosomal miRNAs in stem cell differentiation using Dgcr8-deficient mouse embryonic stem cells (mESCs), which are incapable of producing mature miRNAs. Although the differentiation capacity was markedly impaired in these cells, partial restoration was observed following treatment with exosomes derived from differentiating wild-type mESCs. Exosomal miRNA uptake was confirmed, and gene ontology analysis revealed significant enrichment of pathways associated with cell fate determination, morphogenesis, and apoptosis regulation. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that exosomal miRNAs modulated multiple osteoinductive signaling cascades, notably the MAPK and TGF-β pathways, in Dgcr8-deficient cells. Apoptotic markers were also downregulated, suggesting a protective effect conferred by the exosomal cargo. Collectively, our results suggest that exosome-mediated delivery of miRNAs may represent a fundamental mechanism by which pluripotent stem cells coordinate stress responses and differentiation trajectories, providing novel insights into the regulation of embryogenesis. Full article

Background: Cardiovascular complications stemming from diabetes pose a grave threat to patients’ survival. Both type 1 diabetes (T1D) and type 2 diabetes (T2D) significantly increase the risk of heart failure, yet no reports have clarified whether there are differences in the pathway alterations involved in these two conditions. Investigating the heterogeneity of the cardiac remodeling between these two types of diabetes is conducive to reducing the incidence of cardiovascular events in diabetic patients in clinical practice. Methods: T1D and T2D models were established in adult mice, and the hearts were collected for RNA sequencing. Differential expression analysis (DEA) was performed. Integrating functional enrichment analyses, we probed into gene and pathway heterogeneity. Subsequently, we compared single-cell RNA sequencing (scRNA-seq) data of hearts from T1D and T2D mice, focusing on three cell populations (endothelial cells, macrophages, and fibroblasts) to identify gene and pathway differences. Finally, we evaluated shared genes and common signaling pathway changes across these three cell populations in both diabetes types. Results: We have successfully established T1D and T2D models in mice. Compared with shared genes, the two types of diabetes had more consistent pathway changes. Further scRNA-seq analysis identified endothelial cells, macrophages, and fibroblasts as significantly associated with the diabetic phenotype. In shared pathway, endothelial cells were significantly enriched in pathways related to endothelial proliferation and angiogenesis; macrophages were enriched in immune response pathways; and fibroblasts were enriched in pathways involving fibrosis, cell proliferation, and apoptosis. In endothelial cells, inflammatory response and fatty acid metabolism pathways were predominantly enriched in T1D, while energy metabolism pathways were dominant in T2D. In macrophages, antiviral immune pathways were specifically enriched in T1D, whereas macrophages in T2D were additionally implicated in the regulation of cardiomyocyte function. In fibroblasts, immune-related pathways were characteristically enriched in T1D, while cell respiration and energy supply pathways were prominent in T2D. Common functional enrichment pathways across the three cell types in both diabetes types mainly involved innate immune responses and cardiac morphogenesis, with the proportion of shared pathways being significantly higher than that of shared genes. Conclusions: This study, by combining RNA sequencing and scRNA-seq, revealed that cardiac pathologies induced by T1D and T2D exhibit a higher degree of consistent pathway changes compared to shared gene changes. Interventions targeting these common pathways may hold greater value in preventing and treating diabetic cardiomyopathy. Full article

Soybean (Glycine max (L.) Merr.) is a globally important legume crop valued as a major source of plant-based protein and edible oil. Understanding the transcriptional programs underlying tissue-specific development is essential for improving seed quality and agronomic performance. Here, we present an integrative transcriptomic analysis of soybean based on 12 samples representing key seed developmental stages—including globular, heart, cotyledon, embryo, dry seed, mid-mature, and late-mature—and vegetative and reproductive tissues, including leaf, root, stem, flower bud, and seedling at 6 days after imbibition (6 DAI). Following data preprocessing and filtering, 54,880 genes were retained for downstream analysis. Principal component analysis revealed clear separation between seed and non-seed tissues, indicating that tissue identity is the dominant driver of transcriptomic variation. Analysis of the top 100 most variable genes further highlighted distinct expression modules associated with seed maturation and vegetative growth. Differential expression analysis identified 9785 genes exhibiting significant expression differences between seed and non-seed tissues, including 1139 upregulated and 8646 downregulated genes under relaxed statistical thresholds. Functional characterization of seed-upregulated genes revealed enrichment of biological processes related to storage metabolism, embryo development, and stress protection mechanisms associated with desiccation tolerance. In addition, co-expression network and correlation analyses demonstrated strong transcriptional coherence among seed tissues and distinct clustering of vegetative organs. Together, these results provide a comprehensive systems-level overview of transcriptional organization across soybean tissues and identify candidate gene sets relevant to seed biology, functional genomics, and crop improvement. Full article

Cinnamoyl-CoA reductase (CCR) is the first rate-limiting enzyme in the lignin biosynthetic pathway in higher plants. It catalyzes the conversion of cinnamoyl-CoA into the corresponding cinnamaldehydes. Tea plant (Camellia sinensis) is a perennial woody species. Systematic identification and functional characterization of the CCR gene family in tea plants is still limited. In this study, 202 CCR genes were identified from six tea plant cultivars, and a significant expansion of the CCR gene family was observed during the domestication process from wild to cultivated tea plants. A total of 50 CsCCR genes were identified in the tea cultivar ‘Shuchazao’, and they were distributed across 13 chromosomes. Multiple sequence alignment revealed that the key catalytic motifs NWYCYGK and H-X-X-K were fully conserved in CsCCR1, CsCCR2, and CsCCR3. Phylogenetic analysis showed that CsCCR1/2/3 clustered with AtCCR1/2 and PtrCCR2, which were known to be involved in lignin biosynthesis. Transcriptome data analysis showed that CsCCR3 exhibited significantly higher transcript abundance in stems than in young, mature, and old leaves. CsCCRL9, CsCCRL33, CsCCRL34, and CsCCRL36 also showed relatively high expression levels in stem. RT-qPCR further confirmed the high expression of CsCCR3 and CsCCRL33 in stems. Furthermore, comparison of CCR members derived from tandem and segmental duplication in the tea cultivar ‘Shuchazao’ showed clear differences in Ka/Ks ratios, expression correlations, and the distribution of stress-responsive cis-acting elements. This study provides new insights into the expansion and duplication-related functional divergence of the CCR gene family in tea plant and identifies key candidate genes potentially involved in lignin biosynthesis and stress responses. Full article

Large-scale expansion of human mesenchymal stem cells (hMSCs) remains a major challenge due to the intrinsic trade-off between cell proliferation and the maintenance of multipotency in conventional culture systems. Stiff substrates, such as tissue culture polystyrene or rigid hydrogels, promote rapid proliferation but induce progressive loss of stemness, whereas very soft matrices preserve multipotency at the expense of cell growth. To overcome this limitation, we developed mechanically soft, phase-separated gelatin–phenol/hyaluronic acid–phenol (Gtn-Ph/HA-Ph) hydrogels with precisely controlled microstructures via enzyme-mediated crosslinking. These hydrogels consist of HA-rich, dot-like domains embedded within a continuous Gtn-rich network, allowing for independent tuning of stiffness and domain architecture. On single-component Gtn-Ph hydrogels, hMSC proliferation increased with substrate stiffness, whereas soft hydrogels with a storage modulus (G′) of approximately 0.6 kPa markedly suppressed proliferation while preserving stemness marker expression, confirming the stiffness-dependent trade-off. In contrast, phase-separated Gtn-Ph/HA-Ph hydrogels supported robust hMSC proliferation even under soft mechanical conditions while maintaining high expression of stemness-associated markers. During long-term culture, hMSCs achieved a 68- to 195-fold increase in cumulative cell yield on soft Gtn-Ph/HA-Ph hydrogels (G′ = 0.5 kPa) compared with tissue culture polystyrene. Expression of α-smooth muscle actin (α-SMA) mRNA, encoded by the ACTA2 gene and associated with cellular senescence and fibrotic activation, was completely suppressed, while hMSCs retained robust adipogenic, osteogenic, and chondrogenic differentiation capacities. These results demonstrate that phase-separated Gtn-Ph/HA-Ph hydrogels effectively resolve the proliferation–multipotency dilemma in hMSC expansion and provide a promising platform for scalable manufacturing of therapeutic stem cells. Full article

Cultured urine-derived cells (UDCs) have been proposed as a source of material for the RNA-based molecular diagnosis of genetic disorders. Previous studies have shown that UDCs can be clonally expanded, passaged, frozen, regrown and have some stem cell characteristics, but their anatomic origin and diagnostic utility remain insufficiently explored. In this study, we cultured UDCs from 40 individuals (aged 4 to 20 years; 21 females) and extracted RNA for sequencing. We compared UDC gene expression to that of marker genes of the kidney and urinary tract segments. UDC gene expression most closely matched marker genes of parietal epithelial cells that line the inner surface of Bowman’s capsule in the kidney glomerulus. UDCs expressed VCAM1 (CD106) and POUF51 (OCT4), consistent with a progenitor cell type. UDCs also expressed 54.4% of 3125 OMIM-listed disease-causing genes. This indicated that UDCs can be used to diagnose a similar number of genetic disorders as skin fibroblasts and a wider range of genetic disorders than can be analysed by RNA extracted from whole blood. In conclusion, UDCs are a non-invasive cell source for RNA sequencing that is suitable for investigating a broad range of conditions. Full article

Rheumatoid arthritis (RA) is a chronic autoimmune rheumatic disease of unknown etiolgy, characterized by erosive polyarthritis that leads to joint destruction and systemic inflammatory lesions in internal organs. Pain is a primary symptom of RA and a major contributor to psychological disturbances, which influence patients’ subjective evaluation of their condition. These psychological issues may stem from disruptions in central pain regulation mechanisms, such as central sensitization (CS), which can also affect central metabolic processes. The objective was to investigate how the severity of central sensitization, measured by the Central Sensitization Inventory (CSI) questionnaire (Part 1), impacts clinical and neuropsychiatric parameters, as well as the expression of genes related to inflammation, tissue destruction, carbohydrate metabolism, and fatty acid metabolism in peripheral blood mononuclear cells (PBMCs) in patients with RA. Methods involved collecting blood samples from 59 RA patients (mean age 52.0 years). Clinical status was assessed using the DAS28 index and serum levels of CRP, ASPA, and RF. Neuropsychiatric parameters were evaluated through questionnaires measuring CS severity score (CSI), pain intensity (VAS, BPI), neuropathic pain (PainDETECT), anxiety and depression (HADS), fatigue (FSS, FACIT-F), fibromyalgia symptoms (FIRST), and pain catastrophizing. Protein expression in PBMCs was measured by ELISA, while gene expression was analyzed using quantitative real-time RT-PCR. All patients exhibited moderate to high disease activity. Participants were divided into four subgroups according to their CSI scores: subclinical (0–29 points), mild (30–39 points), moderate (40–49 points), and severe/extreme (50–100 points). Higher CSI scores correlated with significant increases in neuropsychiatric symptoms and a notable decrease in vitality. However, clinical parameters showed no significant differences among the subgroups. Gene expression analysis revealed upregulation of genes involved in the pentose phosphate pathway (G6PD), antioxidant defense (SOD1), fatty acid metabolism (FASN, CPT1B), apoptosis (CASP3), and tissue destruction and hypernociception (MMP-9) compared to healthy controls. The pro-inflammatory cytokine IL-1β expression was comparable to controls, while TNFα expression was elevated only in patients with severe/extreme CS scores. These findings suggest that CS-related disturbances may contribute to increased disease severity in RA, even in patients receiving active antirheumatic treatment. At the cellular level, disease severity appears linked to dysregulated expression of genes governing central metabolic processes, despite low expression of pro-inflammatory cytokine genes. Full article

Bacterial wilt caused by Ralstonia solanacearum is a major constraint on tomato (Solanum lycopersicum L.) production, yet the molecular basis of quantitative resistance remains poorly understood. In this study, comparative transcriptome profiling was performed on resistant (‘ZM3’) and susceptible (‘ZM86’) tomato inbred lines following pathogen inoculation in roots, stems, and leaves. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were conducted to identify resistance-associated regulatory modules and hub genes. The results revealed distinct gene expression patterns between the two genotypes after infection. Several co-expression modules were significantly associated with resistance or susceptibility traits. Functional enrichment analysis showed that differentially expressed genes were mainly involved in plant hormone signal transduction, plant–pathogen interaction, phenylpropanoid biosynthesis, and cell wall modification. Genes related to ethylene and salicylic acid signaling were strongly induced following infection, whereas brassinosteroid-associated genes showed genotype-dependent expression patterns. Network analysis further identified several hub genes within defense-related modules, including ACO (Solyc04g007980), ERF1 (Solyc09g091950), MAPK9, receptor-like kinase RLK (Solyc07g006770), and a dirigent family gene (Solyc10g008900). Taken together, our results suggest that tomato resistance to Ralstonia solanacearum involves a coordinated defense network integrating hormone-mediated transcriptional regulation and structural reinforcement, and provides candidate genes for breeding bacterial wilt-resistant cultivars. Full article

The unique ecological gradients of Xinjiang have fostered a rich reservoir of genetic resources in local sheep populations. However, the population genetic structure, adaptive mechanisms to extreme environments, and the genetic basis underlying key economic traits of these breeds remain poorly understood. To address this gap, we performed whole-genome resequencing of 140 individuals from seven indigenous sheep populations—Altay, Bayinbuluke, Kazakh, Kirgiz, Bashibai, Turpan Black, and Yemule White—identifying 18,700,507 high-quality SNPs. Genetic diversity analyses revealed that all populations exhibited comparable levels of genetic diversity, with modest variation across breeds, with Turpan Black sheep exhibiting the highest observed heterozygosity (Ho = 0.3110) and proportion of polymorphic sites, whereas Kirgiz sheep showed comparatively lower values. Population structure analyses consistently indicated that geographic isolation is the primary driver of genetic differentiation, with Kirgiz sheep from the Pamir Plateau in southern Xinjiang displaying the greatest genetic distance relative to northern Xinjiang populations. By integrating multiple selection signature detection methods—including F_ST, π ratio, and XP-CLR—we found that genes under selection in Kirgiz sheep were significantly enriched in biological pathways related to stem cell pluripotency regulation (e.g., BMPR1B), DNA repair (e.g., DDB2), and neural development, thereby elucidating their unique genetic adaptations to high-altitude environments. In contrast, Turpan Black sheep appear to cope with heat stress through mechanisms involving basal transcriptional regulation (e.g., GTF2I), maintenance of protein homeostasis (e.g., DNAJB14), and melanin biosynthesis (e.g., MC1R). Furthermore, comparative analysis of body size identified a suite of candidate genes associated with growth and development (e.g., CUX1, KIT), which are primarily involved in transcriptional regulation, protein kinase activity, and the ubiquitin-mediated proteolytic system, thereby revealing a multi-layered genetic regulatory network governing body conformation. Collectively, this study provides a comprehensive genomic framework for understanding the genetic structure, adaptive evolution, and molecular basis of economically important traits in indigenous sheep breeds from Xinjiang, offering valuable candidate targets for future functional validation and precision breeding programs. Full article