Search Results (70,371)

This study was conducted to evaluate the effects of chia seed oil (CSO; Salvia hispanica L.) on the growth performance, haematological-biochemical parameters, immune-related gene expression, and disease resistance to Aeromonas hydrophila in common carp (Cyprinus carpio). The fish were fed diets containing 0%, 0.5%, 1%, and 2% CSO for 60 days. The results showed a significant improvement in final weight, specific growth rate (SGR), and feed conversion ratio (FCR) in fish fed diets containing 1% and 2% CSO compared to the control group. Haematocrit (Hct) and haemoglobin (Hb) levels increased in the CSO groups, while serum triglyceride and cholesterol levels decreased significantly, particularly in the 1% CSO group. The observed decrease in liver enzyme activities (AST, ALT) suggested a hepatoprotective effect of CSO. In the stress test with A. hydrophila, the highest survival rate (80%) was recorded in the 2% CSO group. Furthermore, gene expression analyses performed on spleen tissue revealed an increase in the expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-8 in the groups fed with CSO, particularly at the 1% level. These findings indicate that adding 1–2% CSO to carp feed promotes growth, improves lipid metabolism, strengthens immune status, and increases resistance to bacterial infection. Consequently, the use of CSO as a sustainable and functional additive to fish oil in fish feed is suggested. Full article

Fibrosis manifests as an excessive accumulation of fibrillar collagen in tissues where secreted collagen exceeds degradation. Myofibroblasts are important contributors to the excessive collagen seen in fibrotic lesions. Accordingly, targeting signaling pathways that enhance collagen degradation and subdue myofibroblast differentiation has the potential to optimize collagen remodeling and improve organ fibrosis. One of the most promising molecular targets for therapeutic development is the G protein-coupled receptor (GPCR) family, which is diverse, cell-type-specific, multi-pass transmembrane receptors that participate in the regulation of extracellular matrix remodeling. GPCRs are categorized into multiple subclasses, some of which activate signaling cascades that can augment or reduce pro-fibrotic processes, depending on which Gα class is activated. Specifically, activation of Gαs GPCR stimulates production of the second messenger, cyclic adenosine monophosphate (cAMP), which generally inhibits pro-fibrotic mediators. A related, second approach for control of fibrosis is the blockade of a specific mechanosensitive, Ca²⁺-permeable channel that is implicated in fibrosis and contributes to myofibroblast differentiation, the transient receptor potential vanilloid type 4 (TRPV4). In health, TRPV4 activation regulates collagen remodeling, but when dysregulated, it promotes pro-fibrotic gene expression through mechanosensitive transcription factors. In this review, we focus on the functions of the Gαs GPCR pathway and TRPV4 activation through the interplay of the second messengers cAMP and Ca²⁺ ions. Ca²⁺ influx modulates cAMP levels by regulating phosphodiesterases and adenylyl cyclases. We consider evidence that Gαs GPCR and TRPV4 signaling pathways interact antagonistically to either promote collagen degradation or to increase the formation of myofibroblasts through signaling that involves cAMP and Ca²⁺ conductance. Coordinated activation of the Gαs GPCR pathway and inhibition of TRPV4 could provide a novel, bimodal approach to control tissue fibrosis. Full article

This study evaluated the protective effects of naringin (NG) against intestinal injury in 7-day-old piglets infected with porcine epidemic diarrhea virus (PEDV). Eighteen piglets (Duroc × Landrace × Large, body weight = 2.58 ± 0.05 kg) were divided into three treatment groups based on similar body weights and equal numbers of males and females: the blank control group (CON group), the PEDV infection group (PEDV group), and the NG intervention + PEDV infection group (NG + PEDV group) (n = 6 per group). The experiment lasted for 11 days, comprising a pre-feeding period from days 0 to 3 and a formal experimental period from days 4 to 10. On days 4–10 of the experiment, piglets in the NG + PEDV group were orally administered NG (10 mg/kg). On Day 8 of the experiment, piglets in the PEDV and NG + PEDV groups were inoculated with PEDV (3 mL, 10⁶ 50% tissue culture infective dose (TCID₅₀) per milliliter). On day 11 of the experiment, piglets were euthanized for sample collection. PEDV infection caused significant intestinal damage, including a decreased (p < 0.05) villus height in the duodenum and ileum and an increased (p < 0.05) crypt depth in all intestinal segments. This intestinal damage was accompanied by an impaired absorptive function, as indicated by reduced (p < 0.05) serum D-xylose. Further results showed that PEDV compromised the intestinal antioxidant capacity by decreasing (p < 0.05) glutathione peroxidase and catalase activities, and it stimulated the intestinal inflammatory response by upregulating (p < 0.05) the expression of key inflammatory genes, including regenerating family member 3 gamma (REG3G; duodenum, jejunum, colon), S100 calcium binding protein A9 (S100A9; ileum, colon), interleukin 1 beta (IL-1β; ileum, colon), and S100 calcium binding protein A8 (S100A8; colon). PEDV also suppressed the intestinal lipid metabolism pathway by downregulating (p < 0.05) the ileal expression of Solute Carrier Family 27 Member 4 (SLC27A4), Microsomal Triglyceride Transfer Protein (MTTP), Apolipoprotein A4 (APOA4), Apolipoprotein C3 (APOC3), Diacylglycerol O-Acyltransferase 1 (DGAT1), and Cytochrome P450 Family 2 Subfamily J Member 34 (CYP2J34). Moreover, PEDV suppressed the intestinal antiviral ability by downregulating (p < 0.05) interferon (IFN) signaling pathway genes, including MX dynamin like GTPase 1 (MX1) and ISG15 ubiquitin like modifier (ISG15) in the duodenum; weakened intestinal water and ion transport by downregulating (p < 0.05) aquaporin 10 (AQP10) and potassium inwardly rectifying channel subfamily J member 13 (KCNJ13) in the duodenum, aquaporin 7 (AQP7) and transient receptor potential cation channel subfamily V member 6 (TRPV6) in the ileum, and TRPV6 and transient receptor potential cation channel subfamily M member 6 (TRPM6) in the colon; and inhibited intestinal digestive and absorptive function by downregulating (p < 0.05) phosphoenolpyruvate carboxykinase 1 (PCK1) in the duodenum and sucrase-isomaltase (SI) in the ileum. Notably, NG effectively counteracted these detrimental effects. Moreover, NG activated the IFN signaling pathway in the jejunum and suppressed PEDV replication in the colon. In conclusion, NG alleviates PEDV-induced intestinal injury by enhancing the antioxidant capacity, suppressing inflammation, normalizing the expression of metabolic and transport genes, and improving the antiviral ability. Full article

Serine proteases represent a significant family of proteolytic enzymes, characterized by their serine-dependent catalytic mechanism. These enzymes are integral to various biological processes, including fungal growth, development, and pathogenicity. Despite their importance, the sequence characterization and expression patterns of this protein family in Setosphaeria turcica are not yet fully characterized and remain underexplored. A total of 74 putative serine protease family proteins (StSPs) were identified in S. turcica and classified into 12 subfamilies based on phylogenetic analysis. Structural domain analysis revealed that 24 StSPs contain signal peptides, of which five were experimentally validated as secretory proteins through yeast secretion assays. Expression profiling using RNA-seq data demonstrated that StSPs exhibit distinct expression patterns across different developmental and infection stages, with 61 genes showing high expression during critical infection phases. The expression levels of nine genes were validated via qRT-PCR, and the results were consistent with the RNA-seq data. Among these proteins, StSP8-4 demonstrated elevated expression during the course of fungal infection. Functional characterization of StSP8-4 OE and RNAi strains revealed that this gene plays a crucial role in maintaining fungal pathogenicity, although silencing did not impair conidium or hyphal development. These findings provide valuable insights for further research on serine protease genes in S. turcica. Full article

Chlorophyll and carotenoid biosynthesis are essential metabolic processes in horticultural plants, critically influencing the coloration and economic value of fruits and petals. However, the regulatory mechanisms that coordinate the accumulation of both chlorophyll and carotenoids are still poorly understood. In this study, we demonstrated that the transcription factor TeSEP4 modulated petal color in marigolds by simultaneously modulating chlorophyll and carotenoid metabolic pathways. Overexpression of TeSEP4 produced dark-yellow petals, which were associated with enhanced carotenoid biosynthesis and suppression of chlorophyll biosynthesis. In contrast, silencing TeSEP4 triggered a shift toward yellow-green petals by reducing carotenoid accumulation while concurrently increasing chlorophyll content. Transcriptome and qRT-PCR analyses further revealed that TeSEP4 overexpression upregulated key carotenogenic genes such as TePSY1 and TePSY3, while downregulating chlorophyll-related genes, including TeCHLH, TeCHL27-1, and TePORA1. Silencing TeSEP4 expression caused the opposite changes in these genes. These findings reveal a transcriptional factor that coordinates chlorophyll and carotenoid biosynthesis, offering a strategy to simultaneously improve carotenoid content and modify petal color in marigolds. Full article

Acinetobacter baumannii (A. baumannii) is an opportunistic pathogen associated with healthcare-related infections and is of particular concern due to its high level of antibiotic resistance and its ability to form biofilms. The global emergence of carbapenem-resistant A. baumannii highlights the urgent need for alternative therapeutic strategies. This study investigated the antibacterial and antibiofilm activities of two scorpion venom-derived peptides, pantinin-1 and pantinin-2, against a reference strain and a clinical isolate of A. baumannii. We found that both peptides, in the non-cytotoxic concentration range, have strong bactericidal activity, showing a minimum inhibitory concentration (MIC) of 6.25 μM and 12.5 μM for pantinin 1 and 2, respectively. Scanning electron microscopy (SEM) analysis showed that the peptides cause extensive damage to the bacterial membrane. Furthermore, both peptides showed potent antibiofilm activity, inhibiting adhesion and maturation, arresting biofilm expansion, and reducing the expression of key biofilm-associated genes (bap, pgaA, and smpA). Altogether, these findings indicate that pantinin-1 and pantinin-2 act through a dual mechanism, combining bactericidal and antivirulence activities. Their strong efficacy at low micromolar concentrations, together with low cytotoxicity, underscores their potential as innovative therapeutic candidates against infections caused by carbapenem-resistant, biofilm-forming A. baumannii. Full article

Background: Osimertinib is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) with high efficacy in treating patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations. Although osimertinib is a frontline anticancer agent for NSCLC, several patients inevitably develop tumor recurrence caused by osimertinib resistance. The activation of anexelekto (AXL) or fibroblast growth factor receptor 1 (FGFR1) is reported as a major factor driving osimertinib resistance in NSCLC. Thus, targeting AXL and FGFR1 offers the potential to overcome osimertinib resistance. Methods: In this study, we generated osimertinib-resistant cell lines from EGFR-mutant NSCLC cell lines in vitro and investigated the biological significance of AX-0085 on these cell lines by conducting transcriptomic analyses. Results: The expression of several genes associated with MAPK, ERK, and FGF receptor signaling pathways, including AXL, was altered upon AX-0085 treatment of osimertinib-resistant cells. Furthermore, AX-0085 treatment effectively blocked AXL and FGFR1 activation and sensitized osimertinib-resistant cells. Additionally, AX-0085 inhibited AXL and FGFR1-dependent oncogenic events, including cell proliferation, clonogenicity, and migration. Conclusions: The dual inhibition of AXL and FGFR1 by AX-0085 can overcome acquired osimertinib resistance, supporting its potential as a therapeutic strategy for treating patients with osimertinib-resistant tumors. Full article

Breast cancer remains the most common malignancy worldwide and the leading cause of cancer-related mortality. Recently, extracellular vesicles (EVs) derived from adipose tissue-derived stem cells (ADSCs) have attracted increasing attention for their potential to modulate inflammatory signaling and influence tumor cell behavior. This in vitro study was designed to investigate the effects of ADSC-EVs on MCF-7 breast cancer cells. EVs were isolated from ADSC culture supernatants and applied to MCF-7 cells at concentrations ranging from 0 to 80% (v/v). Cell viability, migration, and expression of IL-6/STAT3 pathway-related genes were evaluated using MTT, scratch assays, and qRT-PCR. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test, with significance set at p < 0.05. The results showed that 20% EV treatment markedly inhibited MCF-7 cell activity, significantly reducing viability and almost completely blocking migration, with wound closure rates of 35.4% ± 3.80 at 24 h and 47.6% ± 4.2 at 48 h, compared with 48% ± 4.6 and 67% ± 4.2 in the control group, respectively. Notably, expression levels of IL-6, IL-6RST, and STAT3 were significantly downregulated (fold changes 0.155 ± 0.02 and 0.258 ± 0.012, p < 0.01), accompanied by severe disruption of the microtubule network. Immunofluorescence imaging revealed a disorganized microtubule architecture and irregular filament distribution in EV-treated cells, corresponding with decreased expression of TubA1 and CALR genes. These findings indicate that ADSC-EVs not only suppress IL-6/STAT3 inflammatory signaling but also destabilize the intracellular microtubule system, collectively contributing to the inhibition of MCF-7 breast cancer cell migration and survival. This provides an important molecular basis for developing novel EV-based therapeutic strategies in breast cancer treatment. Full article

Background: The phytoene desaturase gene is a classical visual marker for validating CRISPR/Cas9 genome editing in plants, as its loss of function produces a readily scorable albino phenotype. While the biochemical basis of pigment loss is well established, it remains unclear whether pds knockout elicits transcriptomic changes extending beyond carotenoid biosynthesis. Resolving this question is essential for correctly interpreting pds-based editing outcomes and for assessing the robustness of phenotype-only screening approaches. Methods: A CRISPR/Cas9 editing platform targeting pds was established in diploid potato. Albino, non-albino edited, and wild-type tissues were subjected to RNA-seq profiling. Differential expression, functional enrichment, and weighted gene co-expression network analysis were integrated to resolve phenotype-associated transcriptional modules, and hierarchical regulatory layers underlying albinism. Results: CRISPR/Cas9-mediated disruption of pds in potato-generated stable albino phenotypes and revealed extensive transcriptomic reprogramming that was not limited to pigment loss. Albino tissues exhibited more than 9700 differentially expressed genes relative to both wild-type and non-albino edited tissues, whereas non-albino edits showed substantially fewer changes. Functional enrichment demonstrated pervasive suppression of photosynthesis and carbon metabolism alongside activation of secondary metabolism, stress responses, hormone signaling, and cell wall remodeling. WGCNA and cross-validation resolved these changes into distinct, phenotype-associated regulatory layers: MEorangered4 captured coordinated repression of starch and sucrose metabolism (r = −0.998), MEdarkgreen marked albino-linked activation of secondary metabolism and barrier biogenesis (r = 0.855; overlap with Albino Core set, OR = 23.65), while MEblack and MEgrey60 reflected downregulation of stress signaling, proteostasis, and hormone-integrative control and were enriched in transgenic–background-associated gene sets. Conclusions: pds knockout in potato is accompanied by broad transcriptomic changes beyond pigment biosynthesis, suggesting that albinism involves coordinated regulatory and metabolic adjustment under plastid dysfunction rather than pigment loss alone. These results refine the use of pds as a visual editing marker and provide a framework for linking localized genome edits to coordinated network-level transcriptional responses in plants. Full article

Major histocompatibility complex class I-like related gene A (MICA) is the most polymorphic non-classical HLA gene. MICA proteins are expressed at low levels on the surface of normal cells but are highly expressed on the surface of tumor cells. Its most important biological function is to bind to activating receptors on the surface of natural killer (NK) cells or CD8+ T cells, then activate these immune cells to exert immune killing effects. Multiple studies have shown that the amino acids at specific loci in the MICA molecule can significantly affect its binding ability to NKG2D. The binding strength of MICA-NKG2D significantly affects the anti-tumor effect of NK cells in the body and the prognosis of many tumor patients. However, the strong MICA-NKG2D interaction can trigger negative feedback against this immune response by down-regulating the expression of NKG2D or generating soluble MICA, weakening the overly intense immune response. Therefore, simply evaluating the intensity of the anti-tumor immune response from the perspective of the amino acid polymorphism of MICA affecting its binding ability to NKG2D also has limitations. We review the effects of MICA amino acid polymorphism on the affinity of the NKG2D signal pathway and analyze in detail the specific role of MICA amino acid polymorphism in tumor immunity. The study provides a reference for understanding the mechanism of anti-tumor immune response by NK cells or other immune cells, as well as a theoretical basis for considering the MICA-NKG2D signal axis for anti-tumor immune therapy in future clinical practice. Full article

Background/Objectives: The selection and validation of species-specific housekeeping genes (HKGs) have become increasingly common in functional genomics, with application of quantitative Polymerase Chain Reaction (qPCR) or cDNA-based qPCR (RT-qPCR). Despite the Macrobrachium amazonicum having RNA-seq studies available, there are still no data on the most stable and consistent HKGs for use in relative gene expression analyses. Therefore, the present study aimed to identify and validate seven HKGs in M. amazonicum: Eukaryotic Translation Initiation Factor (EIF), 18S ribosomal RNA (18S), Ribosomal Protein L18 (RPL18), β-actin, α-tubulin (α-tub), Elongation Factor 1-α (EF-1α), and Glyceraldehyde-3-phosphate Dehydrogenase (GAPDH). Methods: The HKGs were identified in the M. amazonicum transcriptome, characterized for identity confirmation, and compared against public databases. Subsequently, RT-qPCR assays were prepared using muscle, hepatopancreas, gills, testis, androgenic gland, and ovary to assess the stability of the HKG markers, employing the comparative ∆Ct, BestKeeper, NormFinder, and GeNorm methods. Results: All candidate HKGs identified showed high similarity with other decapods. Reactions performed with these markers demonstrated high specificity, PCR efficiency, and elevated coefficients of determination. The comprehensive ranking, indicated that no single HKG was stable across all tissues, with HKGs showing the best stability being tissue-specific. The most stable HKGs were RPL18 and 18S. GAPDH, historically used as an HKG, showed the poorest performance in stability ranking for most tissues tested, whereas β-actin was most suitable only for ovarian. Conclusions: These data reinforce the need for species-specific HKG validation and provide an appropriate panel of reference markers for gene expression studies in the M. amazonicum. Full article

Root rot disease severely threatens tropical fruit production, leading to plant mortality and reduced yields; however, the mechanisms of host defense responses and pathogen infection remain poorly understood. In this study, Fusarium acutatum was isolated from diseased Annona squamosa roots and identified through morphological features and ITS phylogeny (99.8% identity). Infection triggered a marked activation of antioxidant defenses, with elevated POD, SOD, PAL, PPO, and CAT activities. Transcriptomic and TMT-based quantitative proteomic analyses identified 23,791 and 74,403 differentially expressed genes (DEGs) and 367 and 609 differentially expressed proteins (DEPs) in root at 5 and 10 days post inoculation, respectively, relative to the control. These DEGs and DEPs were consistently enriched in pathways involving redox regulation, protein synthesis and processing, ubiquitin-mediated proteolysis, phenylpropanoid and flavonoid metabolism, cell wall remodeling, plant–pathogen interaction and MAPK signaling. Integrated transcriptomic–proteomic correlation analysis showed clear positive associations between key defense-related genes and proteins, suggesting that phenylpropanoid metabolism and reactive oxygen species (ROS) scavenging play central roles in resistance. Key genes such as CHI2, CHS, and CYP were strongly induced and validated by qPCR, supporting coordinated activation of the defense systems. Furthermore, F. acutatum exhibited upregulation of 50 pathogenic-related proteins, including 4 cell wall-degrading enzymes (e.g., CBH1, pectate lyase), 5 metabolic regulation or signal transduction enzymes (e.g., gabD, TPI, and ENO) and 3 potential effectors, suggesting coordinated pathogen strategies for host colonization. Collectively, this study provides comprehensive multi-omics insight into the molecular mechanisms underlying A. squamosa defense against F. acutatum and offers candidate targets supported by omics evidence, serving as a theoretical reference for the management of root rot. Full article

The dynamic remodeling of the fungal cell wall depends on a balance between chitin synthesis and degradation. Chitinases are critical for nutrient acquisition, cell wall remodeling, and defense; yet, the upstream regulatory mechanisms controlling chitinase gene expression remain poorly understood. Here, Tandem Affinity Purification–Mass Spectrometry (TAP–MS) with the Penicillium oxalicum Snf1 kinase (PoSnf1) as bait identified the zinc finger transcription factor (TF) PoCon7 as a putative target of the Snf1 kinase complex. This complex comprises the catalytic α subunit Snf1, one of three alternative β subunits Gal83, and the γ subunit Snf4. Although PoCon7 does not directly bind PoSnf1 or PoSnf4, it specifically interacts with PoGal83. Phylogenetic analysis indicates that PoCon7 is a conserved, nuclear-localized C2H2-type TF in filamentous fungi. PoCon7 is likely essential for fungal viability, as only a truncated mutant (con7-B) could be generated, while full deletion was lethal. The con7-B mutant displayed delayed hyphal extension, reduced conidiation, downregulation of developmental genes, and upregulation of cell wall-degrading enzyme (CWDE) genes. DNA Affinity Purification Sequencing (DAP-seq) revealed that PoCon7 binds target gene promoters via the motif 5′-TATTWTTAT-3′. ChIP-qPCR confirmed PoCon7 enrichment at specific sites within the chitinase genes chi18A and chi18C, and the disruption of PoCon7 markedly reduced their expression. Thus, PoCon7 represents the first TF shown to directly regulate chitinase gene expression in filamentous fungi. Full article

Wheat dwarf virus (WDV) is a major constraint to global wheat production, causing severe yield losses and economic disruption. Understanding the molecular basis of wheat–WDV interactions is essential for developing resistant cultivars. Non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are key regulators of gene expression and defence. This study identified ncRNAs involved in wheat responses to WDV, including host lncRNAs, miRNAs, and viral small interfering RNAs (siRNAs) targeting WDV genomic regions. High-throughput sequencing revealed extensive ncRNA reprogramming under WDV infection. A total of 437 differentially expressed lncRNAs (DElncRNAs) and 58 miRNAs (DEmiRNAs) were detected. Resistant genotypes displayed more DElncRNAs (204 in Svitava; 163 in Fengyou 3) than the susceptible Akteur (141). In Akteur, 66.7% of DElncRNAs were downregulated, whereas in Svitava, 56.9% were upregulated. Akteur also exhibited more DEmiRNAs (28) than resistant genotypes (15), with predominant downregulation. A co-expression network analysis revealed 391 significant DElncRNA–mRNA interactions mediated by 16 miRNAs. The lncRNA XLOC_058282 was linked to 298 transcripts in resistant genotypes, suggesting a central role in the host defence. Functional annotation showed enrichment in signalling, metabolic, and defence-related pathways. Small RNA profiling identified 1166 differentially expressed sRNAs targeting WDV, including conserved hotspots and 408 genotype-specific sites in Akteur versus Fengyou 3. Infected plants displayed longer sRNAs, a sense-strand bias, and a 5′ uridine preference, but lacked typical 21–24 nt phasing. These findings highlight the central roles of ncRNAs in orchestrating wheat antiviral defence and provide a molecular framework for breeding virus-resistant wheat. Full article

Background: Phosphorus is an essential nutrient for plant growth and development, playing a multifaceted and vital role in plants. Phosphate Transporter 1 (PHO1) is a class of important functional genes involved in plant phosphorus uptake and transport. We identify PHOSPHATE 1 (PHO1) members in mung beans and investigate their response to low phosphorus stress, thereby aiding in the development of stress-tolerant, high-yielding mung bean varieties. Methods: A bioinformatic analysis was performed, which led to the identification of the PHO1 homologue sequence in mung beans. This analysis also elucidated its gene and protein structural characteristics alongside its phylogenetic relationships. qRT-PCR was used to analyze the expression patterns of genes in roots and leaves in response to conditions of prolonged low-phosphorus and phosphorus-deprivation stress. Results: Total PHO1 homologues were identified in mung beans, which can be grouped into 3 groups (Group I-III). Phylogenetic analysis indicates that VrPHO1s shares closer evolutionary relationships with PHO1 in legumes, and exhibits 6 collinear gene pairs with Glycine max (soybean), all with Ka/Ks ratios below 1, suggesting they have undergone purifying selection. The gene promoter region contains multiple cis-acting elements capable of participating in plant growth and development, stress responses, and plant hormone responses. Expression analysis revealed that more VrPHO1 genes responded to phosphorus stress in roots than in leaves; of these, the expression of VrPHO1; H2, VrPHO1; H3, and VrPHO1; H5 genes was significantly induced by continuous phosphorus-deficient stress. Conclusions: This study provides a comprehensive genome-wide identification of the PHO1 family in mung bean and provides valuable candidate gene resources for the future study of their biological functions and regulatory roles in phosphate-deficient stress. Full article