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Background Trehalose-6-phosphate phosphatases (TPPs), which are encoded by members of the TPP gene family, can improve the drought tolerance of plants. However, the molecular mechanisms underlying the dynamic regulation of TPP genes during drought stress remain unclear. In this study, we explored the function of an Arabidopsis TPP gene by conducting comparative analyses of a loss-of-function mutant and overexpression lines. Results The loss-of-function mutation of Arabidopsis thaliana TPPF , a member of the TPP gene family, resulted in a drought-sensitive phenotype, while a line overexpressing TPPF showed significantly increased drought tolerance and trehalose accumulation. Compared with wild-type plants, tppf1 mutants accumulated more H 2 O 2 under drought, while AtTPPF -overexpressing plants accumulated less H 2 O 2 under drought. Overexpression of AtTPPF led to increased contents of trehalose, sucrose, and total soluble sugars under drought conditions; these compounds may play a role in scavenging reactive oxygen species. Yeast one-hybrid and luciferase activity assays revealed that DREB1A could bind to the DRE/CRT element within the AtTPPF promoter and activate the expression of AtTPPF . A transcriptome analysis of the TPPF -overexpressing plants revealed that the expression levels of drought-repressed genes involved in electron transport activity and cell wall modification were upregulated, while those of stress-related transcription factors related to water deprivation were downregulated. These results indicate that, as well as its involvement in regulating trehalose and soluble sugars, AtTPPF is involved in regulating the transcription of stress-responsive genes. Conclusion AtTPPF functions in regulating levels of trehalose, reactive oxygen species, and sucrose levels during drought stress, and the expression of AtTPPF is activated by DREB1A in Arabidopsis. These findings shed light on the molecular mechanism by which AtTPPF regulates the response to drought stress.

Plant height is a critical agronomic trait closely linked to yield, primarily regulated by Gibberellins (GA) and auxins, which interact in complex ways. However, the mechanism underlying their interactions remain incompletely understood. In this study, we identified a tomato mutant exhibiting significantly reduced plant height. Through gene cloning and bulked segregant analysis (BSA) sequencing, we found that the mutant gene corresponds to the tomato auxin response factor gene SlARF5/MP . Here, we show that overexpression of SlARF5/MP significantly enhances plant height. Additionally, treatment with GA 3 restored the plant height of the mutant to wild-type (WT) levels, indicating that GA content is a key factor influencing plant height. We also observed significant upregulation of GA-biosynthesis genes, including GA2-oxidases GA20ox3 and GA20ox4 , as well as the GA 3 biosynthesis gene GA3ox1 , in SlARF5 -overexpressing plants. Furthermore, we demonstrated that SlARF5 directly binds to SlGA2ox3 , which mediates the conversion of GA 3 to inactive GA, therebyregulating its expression. Our findings suggest that SlARF5 modulates GA 3 metabolism by regulating GA synthesis genes, ultimately leading to alterations in plant height.

Objective To investigate the prevalence and associated factors of oral frailty in older adults with type 2 diabetes, establish a nomogram prediction model, develop an assessment tool for early screening and prevention of oral frailty in this population, and provide scientific basis for the formulation of personalized oral health management strategies. Methods A convenience sampling method was used to select 533 older adults with type 2 diabetes mellitus who visited two tertiary-level general hospitals in Sichuan Province and one tertiary-level general hospital in Hebei Province from April 2024 to June 2025 as the study subjects. They were randomly divided into a training set and a validation set in a 7:3 ratio. A risk prediction model was constructed through analysis, and a nomogram was drawn. The Hosmer-Lemeshow (H-L) test and receiver operating characteristic (ROC) curve were used to evaluate the model’s goodness of fit and predictive performance, respectively. The constructed model was validated through 1,000 bootstrap sampling iterations to assess its predictive efficacy. Results A total of 533 older adults with type 2 diabetes were included in the final analysis. Among them, 246 patients (46.15%) exhibited symptoms of oral frailty. Multivariate logistic regression analysis revealed that age, type of chronic disease, duration of diabetes, HbA1c level, periodontitis, number of natural teeth, difficulty chewing hard foods, and swallowing disorders were associated with the risk of oral frailty in older adults with type 2 diabetes (all P  < 0.05); The area under the ROC curve (AUC) of the predictive model was 0.847( 95%CI: 0.808–0.886), a sensitivity of 72.3%, a specificity of 83.5%, and a maximum Youden index of 0.558. Internal validation showed that the area under the ROC curve for the validation set was 0.831(95%CI:0.768–0.894), with a sensitivity of 82.2% and specificity of 72.4%. The Hosmer-Leme-show test yielded χ² = 13.548, P  = 0.094 (both > 0.05). The calibration curve showed good agreement between the nomogram model and actual observed values. The ROC and DCA decision curves indicated that the nomogram model has good predictive performance and clinical utility. Conclusions The nomogram model developed in this study provides convenience for clinical assessment of the risk of oral frailty in older adults with type 2 diabetes, and helps doctors identify high-risk groups.

Roots are the main organs through which plants absorb water and nutrients. As the key phytohormone involved in root growth, auxin functions in plant environmental responses by modulating auxin synthesis, distribution and polar transport. The Arabidopsis thaliana trehalose-6-phosphate phosphatase gene AtTPPI can improve root architecture, and tppi1 mutants have significantly shortened primary roots. However, the mechanism underlying the short roots of the tppi1 mutant and the upstream signaling pathway and downstream genes regulated by AtTPPI are unclear. Here, we demonstrated that the AtTPPI gene could promote auxin accumulation in AtTPPI -overexpressing plants. By comparing the transcriptomic data of tppi1 and wild-type roots, we found several upregulations of auxin-related genes, including GH3.3 , GH3.9 and GH3.12 , may play an important role in the AtTPPI gene-mediated auxin transport signaling pathway, ultimately leading to changes in auxin content and primary root length. Moreover, increased AtTPPI expression can regulate primary root growth and lateral root elongation under different concentration of nitrate conditions. Overall, constitutive expression of AtTPPI increased auxin contents and improved lateral root elongation, constituting a new method for improving the nitrogen utilization efficiency of plants.

Chromosome-specific identification is a powerful technique in the study of genome structure and evolution. However, there is no reliable cytogenetic marker to unambiguously identify each of the chromosomes in sugarcane ( spp., Poaceae), which has a complex genome with a high level of ploidy and heterozygosity. In this study, we developed a set of oligonucleotide (oligo)-based probes through bioinformatic design and massive synthetization. These probes produced a clear and bright single signal in each of the chromosomes and their eight homologous chromosomes in the ancient species (2 = 8 = 64). Thus, they can be used as reliable markers to robustly label each of the chromosomes in . We then obtained the karyotype data and established a nomenclature based on chromosomal sizes for the eight chromosomes of the octoploid . In addition, we also found that the 45S and 5S rDNAs demonstrated high copy number variations among different homologous chromosomes, indicating a rapid evolution of the highly repeated sequence after polyploidization. Our fluorescence hybridization (FISH) assay also demonstrated that these probes could be used as cross-species markers between or within the genera of and . By comparing FISH analyses, we discovered that several chromosome rearrangement events occurred in , which might have contributed to the basic chromosome number reduction from 10 in sorghum to 8 in sugarcane. Consistent identification of individual chromosomes makes molecular cytogenetic study possible in sugarcane and will facilitate fine chromosomal structure and karyotype evolution of the genus .

Key messageA novel tetraploid S. spontaneum with basic chromosome x = 10 was discovered, providing us insights in the origin and evolution in Saccharum species.Sugarcane (Saccharum spp., Poaceae) is a leading crop for sugar production providing 80% of the world’s sugar. However, the genetic and genomic complexities of this crop such as its high polyploidy level and highly variable chromosome numbers have significantly hindered the studies in deciphering the genomic structure and evolution of sugarcane. Here, we developed the first set of oligonucleotide (oligo)-based probes based on the S. spontaneum genome (x = 8), which can be used to simultaneously distinguish each of the 64 chromosomes of octaploid S. spontaneum SES208 (2n = 8x = 64) through fluorescence in situ hybridization (FISH). By comparative FISH assay, we confirmed the chromosomal rearrangements of S. spontaneum (x = 8) and S. officinarum (2n = 8x = 80), the main contributors of modern sugarcane cultivars. In addition, we examined a S. spontaneum accession, Np-X, with 2n = 40 chromosomes, and we found that it was a tetraploid with the unusual basic chromosome number of x = 10. Assays at the cytological and DNA levels demonstrated its close relationship with S. spontaneum with basic chromosome number x = 8 (the most common accessions in S. spontaneum), confirming its S. spontaneum identity. Population genetic structure and phylogenetic relationship analyses between Np-X and 64 S. spontaneum accessions revealed that Np-X belongs to the ancient Pan-Malaysia group, indicating a close relationship to S. spontaneum with basic chromosome number of x = 8. This finding of a tetraploid S. spontaneum with basic chromosome number of x = 10 suggested a parallel evolution path of genomes and polyploid series in S. spontaneum with different basic chromosome numbers.

Numerous microRNAs (miRs) are dysregulated in non-small cell lung cancer (NSCLC), serving pivotal roles in its formation and progression. miR-625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NSCLC remains poorly understood. In the present study, we aimed to investigate miR-625 expression in NSCLC and its role in regulating NSCLC cell behavior. miR-625 expression in NSCLC tissues and cell lines was detected using reverse transcription-quantitative polymerase chain reaction. The effects of miR-625 overexpression on NSCLC cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR-625 upregulation on NSCLC growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor-suppressing roles of miR-625 in NSCLC were explored in detail. miR-625 expression was determined to be downregulated in NSCLC tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NSCLC. Exogenous miR-625 expression suppressed NSCLC cell proliferation, migration and invasion, and induced apoptosis in vitro. miR-625 upregulation hindered NSCLC tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR-625 in NSCLC cells. The tumor-suppressing effects of HOXB5 silencing were similar to those of miR-625 overexpression in NSCLC cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR-625 in NSCLC cells. miR-625 upregulation directly targeted HOXB5 to deactivate the Wnt/[beta]-catenin signaling pathway in NSCLC cells in vitro and in vivo. miR-625 was determined to be associated with HOXB5 suppression and Wnt/[beta]-catenin pathway deactivation, which in turn inhibited the aggressive behavior of NSCLC cells in vitro and in vivo.

Numerous microRNAs (miRs) are dysregulated in non-small cell lung cancer (NSCLC), serving pivotal roles in its formation and progression. miR-625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NSCLC remains poorly understood. In the present study, we aimed to investigate miR-625 expression in NSCLC and its role in regulating NSCLC cell behavior. miR-625 expression in NSCLC tissues and cell lines was detected using reverse transcription-quantitative polymerase chain reaction. The effects of miR-625 overexpression on NSCLC cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR-625 upregulation on NSCLC growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor-suppressing roles of miR-625 in NSCLC were explored in detail. miR-625 expression was determined to be downregulated in NSCLC tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NSCLC. Exogenous miR-625 expression suppressed NSCLC cell proliferation, migration and invasion, and induced apoptosis in vitro. miR-625 upregulation hindered NSCLC tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR-625 in NSCLC cells. The tumor-suppressing effects of HOXB5 silencing were similar to those of miR-625 overexpression in NSCLC cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR-625 in NSCLC cells. miR-625 upregulation directly targeted HOXB5 to deactivate the Wnt/β-catenin signaling pathway in NSCLC cells in vitro and in vivo. miR-625 was determined to be associated with HOXB5 suppression and Wnt/β-catenin pathway deactivation, which in turn inhibited the aggressive behavior of NSCLC cells in vitro and in vivo.

Lipoxygenases (LOXs) are key enzymes in plant lipid metabolism and stress responses, yet their genomic organization and functional dynamics in Luffa aegyptiaca —a species of culinary, medicinal, and ornamental importance—remain unexplored. Here, we present the first genome-wide identification and characterization of the LOX gene family in L. aegyptiaca , revealing 29 LOX genes, including 14 members of 13S-lipoxygenases (13-LOX) and 15 members of 9S-lipoxygenases (9-LOX), respectively. Notably, tandem duplication events shaped the expansion of LOX genes, with 24 genes clustered in two loci, suggesting functional diversification to enhance environmental adaptability. Phylogenetic analysis demonstrated evolutionary conservation of LOX genes across Cucurbitaceae species, while collinearity analysis highlighted conserved genomic organization. Promoter cis-element profiling identified stress- and hormone-responsive motifs, implicating LOX genes in developmental and stress regulatory networks. Tissue-specific expression patterns revealed 18 LOX genes predominantly expressed in tendril, fruit, root, and male flower, linking them to organ-specific physiological roles. Crucially, under heat stress, 9 out of 11 expressed LOX genes were significantly downregulated, indicating their potential role in thermal stress adaptation through metabolic reconfiguration. This study provides foundational insights into the LOX family’s contribution to L. aegyptiaca ’s resilience and offers genetic targets for breeding strategies to improve stress tolerance in cucurbit crops.