Gene最新文献

{"title":"A novel tRNA-derived fragment tRF-Val-CAC-008 as a diagnostic biomarker and pyroptosis regulator in LSCC","authors":"Hongxia Deng ,&nbsp;Dong Ye ,&nbsp;Shijie Qiu ,&nbsp;Shuang Ye ,&nbsp;Chongchang Zhou ,&nbsp;Shuai Fang ,&nbsp;Yuna Zhang ,&nbsp;Shanshan Gu","doi":"10.1016/j.gene.2025.149967","DOIUrl":"10.1016/j.gene.2025.149967","url":null,"abstract":"<div><h3>Objective</h3><div>Laryngeal cancer is one of the most common malignant tumors of the head and neck, with laryngeal squamous cell carcinoma (LSCC) being the most significant pathological type. Transfer RNA-derived fragments (tRFs) fragments have been implicated in tumor progression through diverse regulatory mechanisms. This study examined the diagnostic value and role of tRF-Val-CAC-008 in LSCC.</div></div><div><h3>Methods</h3><div>Levels of tRF-Val-CAC-008 were quantified in LSCC tissues, plasma, saliva, and cells using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The diagnostic value of tRF-Val-CAC-008 was then assessed using the receiver operating characteristic (ROC) curve. LSCC cells were transfected with mimics or inhibitors of tRF-Val-CAC-008, which increased or decreased its level accordingly. Cell proliferation was evaluated using EdU and the cell counting kit-8 (CCK-8) assays. The level of lactate dehydrogenase (LDH) in LSCC cells was measured using an LDH release assay. Pyroptosis-associated proteins were analyzed by Western blotting (WB).</div></div><div><h3>Results</h3><div>tRF-Val-CAC-008 exhibited significantly higher expression levels in LSCC tissues, plasma and saliva. This higher expression correlated with its pro-proliferative effects and suppression of pyroptosis observed in vitro. In LSCC cells, tRF-Val-CAC-008 mimics promoted cell proliferation and reduced LDH secretion. The expression of gasdermin E (GSDME) and caspase-3 proteins was also decreased by tRF-Val-CAC-008 mimics, which in turn regulated pyroptosis. The ROC curves suggest that combined plasma and saliva tRF-Val-CAC-008 can serve as a diagnostic marker to distinguish LSCC patients from healthy participants.</div></div><div><h3>Conclusions</h3><div>The study concluded that tRF-Val-CAC-008 could act as a diagnostic marker for LSCC; it promotes tumor growth by suppressing pyroptosis and promoting cell proliferation.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"982 ","pages":"Article 149967"},"PeriodicalIF":2.4,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel candidate missense variant in the catalytic domain of USP26 associated with asthenoteratozoospermia","authors":"Seyedeh Zahra Mousavi ,&nbsp;Masomeh Askari ,&nbsp;Ken McElreavey ,&nbsp;Anu Bashamboo ,&nbsp;Najmeh Salehi ,&nbsp;Mandana Rastari ,&nbsp;Zeynab Rokhsattalab ,&nbsp;Bahram Mohammad Soltani ,&nbsp;Mehdi Totonchi","doi":"10.1016/j.gene.2025.149945","DOIUrl":"10.1016/j.gene.2025.149945","url":null,"abstract":"<div><h3>Introduction</h3><div>Teratozoospermia, characterized by abnormal sperm morphology, is a significant factor contributing to the male infertility. Deubiquitinating enzymes play a crucial role in controlling protein synthesis and degradation during spermatogenesis.</div></div><div><h3>Methods</h3><div>Whole exome sequencing (WES) and the following insilico analysis were performed to detect the associated variant with asthenoteratozoospermia in a consanguineous Iranian family with two affected brothers.</div></div><div><h3>Results</h3><div>WES identified a novel candidate hemizygous missense mutation (chrX-132161044 T &gt; G:NM_031907.2:c.1205A &gt; C, p.Asn402Thr) in the catalytic domain of the <em>USP26</em> (Ubiquitin-Specific Peptidase 26) deubiquitinating enzyme in two affected siblings. The <em>USP26</em> encodes a testis-specific deubiquitinating enzyme which is necessary for normal spermatogenesis and may influence male fertility. The mutation changes asparagine 402 (N) into threonine (T) and was co-segregated with phenotype in other available family members. In-silico predictions indicate that the N402T change not only leads to the absence of <em>a</em> hydrogen bond between the mutant N402T and F430 residues but also causes a reduction in <em>USP26</em> protein stability, potentially resulting in defects in <em>USP26</em> enzymatic activity.</div></div><div><h3>Conclusions</h3><div>Our findings support a potential role for <em>USP26</em> variants contributing to asthenoteratozoospermia.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"982 ","pages":"Article 149945"},"PeriodicalIF":2.4,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145803957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Association of polymorphisms in the interleukin-4 gene with response to hepatitis B vaccine and susceptibility to hepatitis B virus infection: a meta-analysis” [Gene 525 (2013) 35–40]","authors":"Wei Cui,&nbsp;Cui-Ming Sun,&nbsp;Bao-Cheng Deng,&nbsp;Pei Liu","doi":"10.1016/j.gene.2025.149947","DOIUrl":"10.1016/j.gene.2025.149947","url":null,"abstract":"","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149947"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Correlation between TGF-β1-509 C>T polymorphism and risk of digestive tract cancer in a meta-analysis for 21,196 participants” [Gene 505 (2012) 66-74]","authors":"Jian Min Zhang ,&nbsp;Xi Jun Cui ,&nbsp;Yun Qiang Xia ,&nbsp;Sen Guo","doi":"10.1016/j.gene.2025.149948","DOIUrl":"10.1016/j.gene.2025.149948","url":null,"abstract":"","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149948"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Under the dual hit: genetic and phenotypic analysis of a Han family with severe adolescent cirrhosis from the convergence of Wilson’s disease and favism","authors":"Yu-qin Xie ,&nbsp;Zi-yan Xu ,&nbsp;Hong Lin ,&nbsp;Li-jun Xie ,&nbsp;Jie-wei Luo ,&nbsp;Li-jun Zhang ,&nbsp;Zhi-hai Zheng","doi":"10.1016/j.gene.2025.149953","DOIUrl":"10.1016/j.gene.2025.149953","url":null,"abstract":"<div><div>Hepatolenticular degeneration (HLD, MIM:277900) is an autosomal recessive disorder characterized by excessive copper accumulation in hepatocytes, leading to hepatic and neurological abnormalities, hepatocellular injury, neurodegeneration, and copper deposition in the cornea. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common genetic cause of hemolytic anemia, which can be triggered by chronic conditions, drugs, food, or infections, and exhibits highly variable severity. In some cases, multiple genetic factors may collectively influence disease presentation and progression. This study reports a proband who developed abnormal liver function at age 20. Four years later, she exhibited severe jaundice, liver dysfunction, serous effusions, anemia, and Kayser–Fleischer rings, leading to diagnoses including decompensated cirrhosis, splenomegaly, suspected HLD, hemolytic anemia, portal hypertension, hypoproteinemia, low T3 syndrome, primary peritonitis, and gallstones with cholecystitis. Genetic screening identified two pathogenic heterozygous variants in ATP7B (NM_000053.4): c.2128G &gt; A (p.G710S) in exon 8 and c.525dupA (p.V176Sfs*28) in exon 2, together forming a compound heterozygous mutation. Additionally, a heterozygous mutation in G6PD (NM_001360016.2), c.1388G &gt; A (p.R463H) in exon 12, was found. Family members carrying the G6PD variant showed recurrent benign jaundice or remained asymptomatic. A heterozygous missense variant of uncertain significance, c.205C &gt; T (p.R69C), was also detected in exon 3 of STEAP3 (NM_182915.3), a gene linked to hypochromic microcytic anemia with iron overload type 2 (MIM#615234). This rare variant was predicted to be deleterious by in silico tools, suggesting possible genetic cosegregation.</div><div>SWISS-MODEL analysis indicated that these variants may alter the three-dimensional structures of the copper-transporting ATPase and G6PD proteins, potentially impairing function—particularly the frameshift mutation p.V176Sfs*28. We hypothesize that the accumulation of multiple pathogenic genetic factors resulted in a “double-hit” effect, leading to the patient’s severe phenotypes, including advanced liver cirrhosis and hemolytic anemia. Elucidating such multi-gene “double-hit” mechanisms may enhance the understanding of gene–gene interactions in complex diseases.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149953"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trolline attenuates diabetic vascular injury by regulating SLC7A11-mediated ferroptosis and mitochondrial dysfunction","authors":"Wenbo Liu ,&nbsp;Cuifang Lu ,&nbsp;Bin Yang ,&nbsp;Ying Liu ,&nbsp;Jie Yan ,&nbsp;Tingyu Song ,&nbsp;Xiaofei Wang","doi":"10.1016/j.gene.2025.149968","DOIUrl":"10.1016/j.gene.2025.149968","url":null,"abstract":"<div><h3>Aims</h3><div>This study investigated the therapeutic potential of Trolline, a natural compound, for alleviating high-glucose (HG)-induced vascular endothelial ferroptosis and mitochondrial dysfunction via the cystine/glutamate antiporter solute carrier family 7 member 11 (SLC7A11) pathway.</div></div><div><h3>Materials and methods</h3><div>In db/db mice, inflammatory damage; glucose tolerance; and the expression of SLC7A11, glutathione peroxidase 4 (GPX4), and long-chain acyl-CoA synthetase family member 4 (ACSL4) were detected after treatment with Trolline. An HG-induced human microvascular endothelial cell (HMEC-1) injury model was established in vitro. Fe²⁺ deposition and GSH levels serve as important indicators of ferroptosis. The mitochondrial membrane potential and the cytoskeleton were determined by JC-1 and F-actin staining, respectively. The levels of apoptosis, cell cycle and reactive oxygen species (ROS) were determined by flow cytometry. Oxidative stress levels were assessed by measuring malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity. Ferroptosis- and inflammation-related protein expression in HMEC-1 cells was verified by Western blotting.</div></div><div><h3>Results</h3><div>In vivo experiments revealed that Trolline can lower blood sugar levels, alleviate inflammatory damage, and regulate the expression of ferroptosis-related proteins in db/db mice. In vitro experiments demonstrated that Trolline can alleviate various effects induced by HG. Under HG conditions, Trolline can inhibit apoptosis, reverse the cell cycle arrest in the SubG1 phase, reduce oxidative stress levels and Fe²⁺ overload, restore mitochondrial function, promote cytoskeletal remodelling, and regulate the expression of ferroptosis-related proteins. Mechanistically, ferroptosis inhibitors (Ferrostatin-1) and Trolline have the same protective effect on HMEC-1 cells in an HG environment. However, overexpression of SLC7A11 led to loss of the inhibitory effect of Trolline on ferroptosis, which confirms that the effect of Trolline is dependent on the SLC7A11-ferroptosis axis.</div></div><div><h3>Conclusion</h3><div>Trolline can alleviate diabetic vascular damage through SLC7A11-mediated inhibition of ferroptosis, improved mitochondrial function, and reduced oxidative inflammatory damage, providing a basis for the treatment of diabetic vascular complications.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149968"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The expanding role of Furin in human Disease: A comprehensive review","authors":"Xinyang Li ,&nbsp;Chong Liu ,&nbsp;Haidi Hu","doi":"10.1016/j.gene.2025.149969","DOIUrl":"10.1016/j.gene.2025.149969","url":null,"abstract":"<div><div>Furin is a calcium-dependent serine endoprotease that activates multiple substrates by cleaving at polybasic motifs, playing a pivotal role in human physiology and pathology. This review summarizes the latest research progress regarding Furin’s extensive involvement in infectious diseases, tumor diseases, cardiovascular diseases, neurodegenerative diseases, metabolic diseases, and autoimmune diseases. This review offers an in-depth analysis of Furin’s dual functions, which include promoting viral entry into host cells, driving oncogenesis via growth factors, metalloproteinases, and the Notch signaling pathway, and maintaining metabolic homeostasis and immune tolerance. Key pathophysiological mechanisms involve the dysfunction of Furin substrate activation in atherosclerosis, hypertension, Alzheimer’s disease, diabetes, and other disorders. The review also highlights the potential value of Furin as a diagnostic and prognostic biomarker and therapeutic target, while pointing out the challenges encountered in developing its inhibitors.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149969"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innovative minicircle DNA vector encoding pri-miR-375 silences E6 and E7 oncoproteins in HPV16-positive CaSki cells","authors":"D. Pereira ,&nbsp;A.M. Almeida ,&nbsp;J.A. Queiroz ,&nbsp;F. Sousa ,&nbsp;N. Alves ,&nbsp;J.F.A. Valente ,&nbsp;A. Sousa","doi":"10.1016/j.gene.2025.149964","DOIUrl":"10.1016/j.gene.2025.149964","url":null,"abstract":"<div><h3>Background</h3><div>The infection by Human Papillomaviruses (HPV) has long been established as one of the main causes of cervical cancer, with HPV16/HPV18 high-risk types expressing E6/E7 oncoproteins that inhibit p53/pRB tumor suppressor proteins. Therefore, this work focuses on gene therapy, using the innovative minicircle DNA (mcDNA) vector to protect and express the pri-miR-375 in the cancer cell nucleus, ultimately originating the microRNA-375 (miR-375) in the cytoplasm. This miR-375, initially downregulated in cervical cancer cells, can silence HPV E6/E7 transcripts, thereby negatively regulating the expression of these oncoproteins.</div></div><div><h3>Methods</h3><div>The mcDNA-pri-miR-375 vector was successfully constructed, biosynthesized in the host cell, extracted, and purified, followed by several <em>in vitro</em> transfection studies in CaSKi cells (HPV16-infected cervical cancer model) to evaluate the mcDNA-pri-miR-375 effect.</div></div><div><h3>Results</h3><div>FITC-stained-mcDNA-pri-miR-375 was present in cancer cell nucleus, confirmed by confocal microscopy. RT-PCR analysis showed a more intense band of miR-375 transcripts, and RT-PCR/ RT-qPCR confirmed that E6/ E7 transcript levels were nearly 80 % diminished 24 h after CaSki cells transfection. Also, western-blot showed a decreased band intensity for E6/ E7 proteins on transfected cells. Proliferation and cell invasion studies demonstrated growth and migration arrest for CaSki cells throughout 72 h. Cell viability study of these cells also revealed a gradual decrease for the same period, while the NHDF cell viability was not affected, indicating specificity towards CaSki. The consequent effect of silencing the E6/ E7 transcripts was also observed through an increase in p53 protein levels (determined by western blot and ELISA) and caspase-3 activity, after 48 h of CaSki cell transfection.</div></div><div><h3>Conclusions</h3><div>These results suggest that mcDNA-pri-miR-375 vector has the potential to be further explored in gene therapy for the treatment of HPV-caused cervical cancer.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"981 ","pages":"Article 149964"},"PeriodicalIF":2.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic and epigenetic determinants of injury risk and recovery in elite athletes: toward precision sports medicine","authors":"Hao Ding ,&nbsp;Qilu Deng ,&nbsp;Zhenhua Guo","doi":"10.1016/j.gene.2025.149957","DOIUrl":"10.1016/j.gene.2025.149957","url":null,"abstract":"<div><div>Musculoskeletal injuries and interindividual variability in recovery remain critical challenges for sustaining elite athletic performance. Despite advances in diagnostics, training, and rehabilitation, unexplained differences in injury risk and recovery efficiency persist. Growing evidence implicates genetic and epigenetic mechanisms in these disparities, influencing collagen integrity, inflammatory regulation, oxidative stress, and muscle regeneration. Key contributors include single-nucleotide polymorphisms (SNPs) in COL1A1, COL5A1, ACTN3, and IL6, as well as novel loci identified by genome-wide association studies (GWAS). Polygenic risk scores (PRS), which integrate the effects of multiple low-impact variants, enhance prediction compared to single-gene markers. Epigenetic regulators, including DNA methylation and exercise-responsive microRNAs (e.g., miR-206, miR-133a, miR-486), provide a dynamic interface linking genetic predisposition with environmental factors such as training load and nutrition. Integration of genomic data with wearable technologies and artificial intelligence enables real-time monitoring, adaptive recovery, and precision load management. Yet, clinical translation faces challenges including limited population diversity, interpretative complexity, and ethical concerns over data privacy and potential misuse. Advancing precision sports medicine will require multidisciplinary, systems-level strategies that unite molecular insights with practical implementation, ultimately enabling individualized injury prevention, optimized rehabilitation, and the preservation of long-term athlete health and performance.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"980 ","pages":"Article 149957"},"PeriodicalIF":2.4,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inorganic nitrogen sources and light cooperatively stimulate gene regulation for non-photosynthetic phosphoenolpyruvate carboxylase in wheat leaves","authors":"Naoki Yamamoto ,&nbsp;Jingru Jiang ,&nbsp;Haoyu Deng ,&nbsp;Ken-ichi Kurotani ,&nbsp;Jiang Zou ,&nbsp;Zaijun Yang","doi":"10.1016/j.gene.2025.149950","DOIUrl":"10.1016/j.gene.2025.149950","url":null,"abstract":"<div><div>Phospho<em>enol</em>pyruvate carboxylase (PEPC) is a bicarbonate fixation enzyme that is associated with nitrogen metabolism. We previously observed that NO₃^– affected the expression levels of <em>PEPC</em> genes differently in detached wheat leaves. Three types of <em>PEPC</em> isogenes, including the orthologous isogene group (<em>Tappc1b</em>) for C₄-photosynthetic <em>PEPC</em>, exhibited distinct transcriptionally up-regulated patterns from one another. However, it remains unclear which nitrogen compounds exactly trigger the gene expression responses and their light dependency. Here, we investigated the cause of isogene-specific expression responses of <em>PEPCs</em> to different forms of nitrogen supplementation. Detached leaves from wheat seedlings cultivated under a nitrogen-deficient condition were incubated with NO₃^–, NH₄⁺, and urea under both light and dark conditions. Notably, the genes analyzed exhibited markedly different expression patterns across the nitrogen forms under the light condition. <em>Tappc1a</em>, which did non-respond to NO₃^–, was up-regulated by NH₄⁺ exclusively under light. <em>Tappc2</em> was also up-regulated by NO₃^– and NH₄⁺ only under light, and these up-regulations were suppressed under the dark condition. The candidate transcriptional regulator <em>DOF1</em> for <em>Tappc1b</em> in wheat was also up-regulated by NO₃^– only under light condition, but earlier than <em>Tappc1b</em>, implicating a DOF1-mediated transcriptional response of <em>Tappc1b</em> to NO₃^–. Comparison of <em>Tappc1b</em> promoter sequences with that of NO₃^–-responsive maize C₄ <em>PEPC</em> revealed conserved light-responsive elements near the Dof1 binding site. These findings suggest that distinct transcriptional regulatory cascades would exist for non-photosynthetic <em>PEPCs</em> in response to different inorganic nitrogen forms.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"980 ","pages":"Article 149950"},"PeriodicalIF":2.4,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145741963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}