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PLANT MOLECULAR BIOLOGY · 2025 ·Vol. 115 ·期 2 ·1-13 · IF 3.8

Light regulates seed dormancy through FHY3-mediated activation of ACC OXIDASE 1 in Arabidopsis

Liu Yitong,Liu Shuangrong,Jing Yanjun,Li Jialong,Lin Rongcheng

Seed dormancy enables plants to delay germination until conditions are favorable for the survival of the next generation. Seed dormancy and germination are controlled by a combination of external and internal signals, in which light and ethylene act as critical regulators. However, how light and ethylene are interlinked to control these two processes remains to be investigated. Here, we show that ethylene and its precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), promote seed germination under light. Light facilitates the conversion of ACC to ethylene, in which phytochrome B (phyB) and FAR-RED ELONGATED HYPOCOTYL3 (FHY3) are functionally required. ACC oxidases (ACOs) catalyze the conversion of ACC to ethylene, among which ACO1 is specifically and predominantly expressed in imbibed seeds. Ethylene induces FHY3 protein accumulation in imbibed seeds, whereby FHY3 directly binds to ACO1 promoter and specifically mediates light-promoted ACO1 expression. Light promotes ACO1 protein accumulation. Overexpression of ACO1 significantly promotes seed germination, and almost completely restores the dormant defect of fhy3 loss-of-function mutants. In summary, this study reveals an ethylene-responsive regulatory cascade of phyB-FHY3-ACO1 that integrates external light input with internal factors to regulate seed dormancy and germination.

CAS / MDL: 16672-87-0 22059-21-8
研究领域: 植物生物学 · 分子遗传学 · 发育生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA · 2025 ·Vol. 122 ·期 6 ·e2417735122 · IF 9.1

Ethylene-independent modulation of root development by ACC via downregulation of WOX5 and group I CLE peptide expression

Wangshu Mou,Ria Khare,Joanna K. Polko,Isaiah Taylor,Juan Xu,Dawei Xue,Philip Benfey,Bram Van de Poel,Caren Chang,Joseph J. Kieber

In seed plants, the canonical role of 1-aminocyclopropane-1-carboxylic acid (ACC) is to serve as the precursor in the biosynthesis of the phytohormone ethylene, and indeed, ACC treatment is often used as a proxy for ethylene treatment. Increasing evidence suggests that ACC can also act independently of ethylene to regulate various aspects of plant growth and development. Here, we explore the effects of ACC on Arabidopsis thaliana root growth and the mechanisms by which it acts. ACC inhibits growth of the primary root in Arabidopsis seedlings when ethylene signaling is blocked, which becomes evident after 36 h of treatment with ACC. This reduced root growth is in part the result of suppressed cell proliferation in the root meristem resulting from altered expression of a key regulator of stem cell niche activity, WOX5. ACC also promotes lateral root (LR) development, in contrast to ethylene, which inhibits LR formation. Transcriptomic analysis of roots revealed no significant changes in gene expression after 45 min or 4 h of ACC treatment, but longer treatment times revealed a large number of differentially expressed genes, including the downregulation of the expression of a small group of phylogenetically related CLE peptides. Reduced expression of these group 1 CLEs in response to ACC leads to the activation of a transcription factor, LBD18, which promotes LR development. These results suggest that ACC acts to modulate multiple aspects of Arabidopsis root growth independently of ethylene via distinct transcriptional effects in the root meristem and LR precursor cells.

CAS / MDL: 3100-04-7
研究领域: 植物学 · 分子生物学 · 遗传学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Plant Signaling & Behavior · 2022 · IF 2.734

Identification of endophytic fungi with ACC deaminase-producing isolated from halophyte Kosteletzkya Virginica

Xiaomin Wang,Zengyuan Tian,Yu Xi,Yuqi Guo

Seashore mallow (Kosteletzkya virginica), as a noninvasive perennial halophytic oilseed-producing dicot, is native from the Gulf to the Atlantic coasts of the U.S. The purpose of our research was to investigate 1-aminocyclopropane-1carboxylic acid deaminase (ACCD) producing endophytic fungi from K.virginica. A total of 59 endophytic fungal strains, isolated from roots in K.virginica of seedlings, were grouped into 12 genera including in Penicillium, Aspergillus, Fusarium, Trichoderma, Rhizopycnis sp., Ceriporia Donk, Trametes sp., Schizophyllum commune sp., Alternaria, Cladosporium, Cylindrocarpon, and Scytalidium according to sequences of ITS. The ACD activity of 10 endophytic fungi isolated was detected. T.asperellum had the highest ACC deaminase activity among all 10 isolated genera of fungal strains, followed by T. viride. Dry weight and fresh weight of plant, plant height, root length, SOD activity, and chlorophyll content of wheat and soybean inoculated with T.asperellum or T. viride was increased compared with non-inoculated control plants under non salt or salt stress. Further analysis showed that T.asperellum or T.viride strains induced downregulation of the expression of ethylene synthesis-related genes such as ACC oxidase (ACO) and ACC synthase (ACS), thereby reducing ethylene synthesis and damage to plants under salt stress. These endophytic fungi can be used as alternative bioinoculants to increase crop yield in saline soil.

CAS / MDL: 119-26-6
研究领域: 植物科学 · 微生物学 · 农业生物技术
✓ 已验证 产品关联 DOI PubMed 高影响因子
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PLANT PHYSIOLOGY · 2024 · IF 6.5

ACC SYNTHASE4 inhibits gibberellin biosynthesis and FLOWERING LOCUS T expression during citrus flowering

Chu Le-Le,Zheng Wei-Xuan,Liu Hai-Qiang,Sheng Xing-Xing,Wang Qing-Ye,Wang Yue,Hu Chun-Gen,Zhang Jin-Zhi

Flowering is an essential process in fruit trees. Flower number and timing have a substantial impact on the yield and maturity of fruit. Ethylene and gibberellin (GA) play vital roles in flowering, but the mechanism of coordinated regulation of flowering in woody plants by GA and ethylene is still unclear. In this study, a lemon (Citrus limon L. Burm) 1-aminocyclopropane-1-carboxylic acid synthase gene (CiACS4) was overexpressed in Nicotiana tabacum and resulted in late flowering and increased flower number. Further transformation of citrus revealed that ethylene and starch content increased, and soluble sugar content decreased in 35S:CiACS4 lemon. Inhibition of CiACS4 in lemon resulted in effects opposite to that of 35S:CiACS4 in transgenic plants. Overexpression of the CiACS4-interacting protein ETHYLENE RESPONSE FACTOR3 (CiERF3) in N. tabacum resulted in delayed flowering and more flowers. Further experiments revealed that the CiACS4–CiERF3 complex can bind the promoters of FLOWERING LOCUS T (CiFT) and GOLDEN2-LIKE (CiFE) and suppress their expression. Moreover, overexpression of CiFE in N. tabacum led to early flowering and decreased flowers, and ethylene, starch, and soluble sugar contents were opposite to those in 35S:CiACS4 transgenic plants. Interestingly, CiFE also bound the promoter of CiFT. Additionally, GA3 and 1-aminocyclopropanecarboxylic acid (ACC) treatments delayed flowering in adult citrus, and treatment with GA and ethylene inhibitors increased flower number. ACC treatment also inhibited the expression of CiFT and CiFE. This study provides a theoretical basis for the application of ethylene to regulate flower number and mitigate the impacts of extreme weather on citrus yield due to delayed flowering.

研究领域: 植物生物学 · 分子遗传学 · 园艺学
✓ 已验证 DOI PubMed 高影响因子
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EUROPEAN JOURNAL OF PHARMACOLOGY · 2022 · IF 5.195

Gallic acid impairs fructose-driven de novo lipogenesis and ameliorates hepatic steatosis via AMPK-dependent suppression of SREBP-1/ACC/FASN cascade

Yuzhen Lu,Cong Zhang,Yingying Song,Liang Chen,Xin Chen,Guohua Zheng,Yuan Yang,Peng Cao,Zhenpeng Qiu

Accumulating evidence suggests that de novo lipogenesis is a typical characteristic facilitating nonalcoholic fatty liver disease (NAFLD) progression. Gallic acid (GA) is a naturally occurring phenolic acid with metabolic disease-related clinical significance and preclinical benefits. This study aimed to evaluate the anti-steatotic potentials of GA in a fructose-induced NAFLD mouse model featuring a hepatic lipogenic phenotype. The results revealed that GA alleviated hepatic steatosis , oxidative stress , and inflammatory response in fructose-fed mice. Mechanistically, GA treatment restored AMP-activated protein kinase α (AMPKα) phosphorylation, resulting in downregulations of pro-lipogenic factors, including sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthetase (FASN), and acetyl-CoA carboxylase (ACC), in hepatocytes of mice and in vitro . Furthermore, computational docking analysis indicated that GA could directly interact with AMPKα/β subunits to stabilize its activation. These results suggest that GA ameliorates fructose-induced hepatosteatosis by restraining hepatic lipogenesis via AMPK-dependent suppression of the SREBP-1/ACC/FASN cascade. Altogether, this study demonstrates that GA supplement may be a promising therapeutic strategy in NAFLD, especially in the subset with enhanced hepatic lipogenesis.

CAS / MDL: 149-91-7 7660-25-5
研究领域: 代谢生物学 · 肝脏疾病 · 药物研发
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Evidence-based Complementary and Alternative Medicine · 2023 · IF 2.65

Rhinacanthin C Ameliorates Insulin Resistance and Lipid Accumulation in NAFLD Mice via the AMPK/SIRT1 and SREBP-1c/FAS/ACC Signaling Pathways

Zhiqiang Gong,Sha Han,Chenlin Li,Tianxiu Meng,Yu Huo,Xianfu Liu,Yanhong Huang,Lifang Yang

Rhinacanthin C (RC) is a naphthoquinone ester with an anti-inflammatory activity extracted from Rhinacanthus nasutus (L.) Kurz (Rn). It has been proven to improve hyperglycemia and hyperlipidemia, but the prevention and mechanism of RC in nonalcoholic fatty liver disease (NAFLD) are not clear. In the current study, we first extracted RC from Rn using ethyl acetate and identified it by HPLC, MS, and NMR. At the same time, molecular docking analysis of RC with AMPK and SREBP-1c was performed using AutoDock software. In addition, the mouse model of NAFLD was induced by a high-fat diet in vivo, and low, medium, and high concentrations of RC were used for intervention. The results showed that RC significantly reduced the body mass and liver body coefficient of NAFLD mice, inhibited liver inflammation and fat accumulation, and improved insulin resistance. Further studies showed that RC significantly reduced the levels of serum leptin and resistin, upregulated the expression levels of adiponectin and adiponectin receptor in the liver, and inhibited the expression levels of MCP-1, TNF-α, and IL-6. In terms of mechanism, RC upregulates the expression of p-AMPK and SIRT1 and downregulates the expression of p-p65, SREBP-1c, Fas, Acc-α, PPAR-γ, and SCD1. These studies suggest that RC improves insulin resistance and lipid accumulation in NAFLD by activating the AMPK/SIRT1 and SREBP-1c/Fas/ACC pathways, respectively.

研究领域: 药理学 · 分子生物学 · 代谢紊乱 · 肝病学
✓ 已验证 DOI PubMed 高影响因子
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iScience · 2024 · IF 4.6

Lysophosphatidylcholine induced by fat transplantation regulates hyperalgesia by affecting the dysfunction of ACC perineuronal nets

Juan Li,Zhen Li,Yanbo Liu,Yijing Li,Yanqiong Wu,Anne Manyande,Zhixiao Li,Hongbing Xiang

Summary The pathogenesis of hyperalgesia is complex and can lead to poor clinical treatment. Our study revealed that epididymal white adipose tissue (eWAT) from spared nerve injury (SNI) mice is involved in the occurrence of hyperalgesia after adipose tissue transplantation. We also showed that lysophosphatidylcholine (LPC) is enriched in the eWAT of SNI mice using non-targeted metabolomic analysis and verified that the levels of LPC in plasma and the anterior cingulate cortex (ACC) region increased following eWAT transplantation. Based on the immunohistochemistry results, we observed that LPC in the ACC region activated microglia via the TRPV1/CamkⅡ pathway. Meanwhile, the disruption of perineuronal nets (PNNs) around PV + neurons in ACC promoted hyperalgesia, and the loss of PNNs and PV + interneurons might be due to microglial phagocytosis. These findings elucidate the mechanism underlying hyperalgesia from the perspective of lipid metabolite LPC and PNNs and provide potential strategies for the treatment of hyperalgesia.

CAS / MDL: 115066-14-3
研究领域: 神经科学 · 疼痛研究 · 代谢组学 · 免疫组化
✓ 已验证 产品关联 DOI PubMed 高影响因子
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CELLULAR ONCOLOGY · 2026 ·Vol. 49 ·期 2 ·55 · IF 5.6

NR2F2/AGAP2 axis: regulating lipid synthesis to drive AML progression via AMPKα/ACC pathway

Xin Qi,Zhang Henan,Zhao Zheng,Xu Gang,Zhang Jihong

Purpose This study aims to investigate the role of AGAP2 in acute myeloid leukemia (AML), particularly its involvement in lipid metabolic reprogramming and AML progression, and to explore the underlying regulatory mechanisms. Methods AGAP2 expression was analyzed in CD34⁺ cells from AML patients stratified by cytogenetic risk. Functional assays, including knockdown and overexpression of AGAP2, were performed in KG-1 and HL-60 AML cell lines to assess effects on proliferation, apoptosis, differentiation, and lipid metabolism. mRNA sequencing and KEGG pathway analysis were used to identify relevant signaling pathways. Lipid accumulation was evaluated via Filipin III staining. The AMPK pathway activator GSK621 was applied to examine lipid deposition. In vivo tumor growth and survival were studied in a mouse model, and bone marrow infiltration of CD45⁺ cells was analyzed. The transcriptional regulation of AGAP2 by NR2F2 was assessed through promoter binding and functional rescue experiments. Results AGAP2 was highly expressed in CD34⁺ cells from AML patients, with higher levels in the poor-risk group compared to favorable- and intermediate-risk groups. Knockdown of AGAP2 induced apoptosis and differentiation, while its overexpression promoted cell proliferation. KEGG analysis indicated enrichment of differentially expressed genes in the AMPK pathway. AGAP2 was found to inhibit AMPK/ACC pathway activation. Overexpression of AGAP2 increased lipid deposition whereas GSK621 treatment reversed it. In vivo, AGAP2 knockdown suppressed tumor growth, improved survival, and reduced CD45⁺ cell infiltration in bone marrow. Furthermore, NR2F2 bound to the AGAP2 promoter and suppressed its transcription. NR2F2 overexpression reduced lipid accumulation, an effect reversed by AGAP2 overexpression. Conclusion AGAP2 promotes lipid deposition and AML progression by inhibiting the AMPKα/ACC pathway. NR2F2 acts as a transcriptional repressor of AGAP2, thereby attenuating AML development. These findings reveal a novel NR2F2/AGAP2/AMPK/ACC regulatory axis in AML, highlighting potential therapeutic targets for lipid metabolism-based interventions in leukemia. Graphical

CAS / MDL: 9004-67-5
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Frontiers in Plant Science · 2018 · IF 3.677

Ethylene-Induced Hydrogen Sulfide Negatively Regulates Ethylene Biosynthesis by Persulfidation of ACO in Tomato Under Osmotic Stress

Jia Honglei,Chen Sisi,Liu Dan,Liesche Johannes,Shi Cong,Wang Juan,Ren Meijuan,Wang Xiaofeng,Yang Jun,Shi Wei,Li Jisheng

A number of recent studies identified hydrogen sulfide (H2S) as an important signal in plant development and adaptation to environmental stress. H2S has been proven to participate in ethylene-induced stomatal closure, but how the signaling pathways of H2S and ethylene interact is still unclear. Here, we reveal how H2S controls the feedback-regulation of ethylene biosynthesis in tomato (Solanum lycopersicum) under osmotic stress. We found that ethylene induced the production of H2S in guard cells. The supply of hypotaurine (HT; a H2S scavenger) or DL-pro-pargylglycine (PAG; a synthetic inhibitor of H2S) removed the effect of ethylene or osmotic stress on stomatal closure. This suggests that ethylene-induced H2S is a downstream component of osmotic stress signaling, which is required for ethylene-induced stomatal closure under osmotic stress. We further found that H2S inhibited ethylene synthesis through inhibiting the activity of 1-aminocyclopropane-1-carboxylic acid (ACC) oxidases (ACOs) by persulfidation. A modified biotin-switch method (MBST) showed that H2S can induce persulfidation of LeACO1 and LeACO2 in a dose-dependent manner, and that persulfidation inhibits the activity of LeACO1 and LeACO2. We also found that LeACO1 is persulfidated at cysteine 60. These data suggested that ethylene-induced H2S negatively regulates ethylene biosynthesis by persulfidation of LeACOs. In addition, H2S was also found to inhibit the expression of LeACO genes. The results provide insight on the general mode of action of H2S and contribute to a better understanding of a plant’s response to osmotic stress.

研究领域: 植物生理学 · 胁迫生物学 · 分子生物学
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Frontiers in Veterinary Science · 2025 · IF 2.9

Adiponectin receptor agonist reduces broiler hepatic lipid deposition

Wenhao Tan,Kunyu Jiang,Yuhan Zhang,Hang Gao,Xingyi Tang,Sha Jiang

To investigate the effects of AdipoRon on fatty liver syndrome (FLS) in chicken, we used a corticosterone (CORT)-induced fatty liver model in Cobb broilers in vivo and fat emulsion-induced model in Leghorn male hepatoma cells (LMH) in vitro. In the in vivo study, eighteen 33-day-old male Cobb broilers were randomly assigned to three groups: control group (CONT, vehicle), corticosterone-treated group (CORT, 4 mg/kg), and corticosterone with AdipoRon-treated group (CORT-AR, 4 mg/kg and 0.2 mg/kg, 1 time/1 day) for 5 days. The results showed AdipoRon reduced CORT-induced increase in liver crude fat content (p < 0.05), increased protein expressions of peroxisome proliferator-activated receptor α (PPARα) (p < 0.05) and adiponectin (ADPN) (p < 0.05), and suppressed the protein expressions of Acetyl-CoA carboxylase 1 (ACC) (p < 0.05) and phosphorylated c-Jun N-terminal kinase 1 (p-JNK1) (p < 0.05) in the liver. In the in vitro study, LMH cells were divided into control (CN), fat emulsion (FE, 10%), and FE + AdipoRon (4 μM) group (FE-AR). AdipoRon reduced FE-induced lipid accumulation (p < 0.05), decreased the protein expression of ACC and tumor necrosis factor-alpha (TNF-α), and enhanced PPARα, the phosphorylation of adenosine 5′-monophosphate-activated protein kinase (AMPK), and carnitine palmitoyl transferase 1 (CPT-1) (p < 0.05). In conclusion, AdipoRon effectively reduces hepatic lipid deposition in CORT-induced FLS broilers, likely through PPARα activation and inhibition of lipid synthesis via ACC downregulation.

CAS / MDL: 50-22-6
研究领域: 兽医学 · 动物营养学 · 分子生物学 · 代谢病学 · 药理学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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FITOTERAPIA · 2026 · IF 2.9

Bioactive constituents of Olea europaea L. leaf extract ameliorate metabolic-associated steatohepatitis via the PPARγ/AMPK/ACC Axis

Xia Zhang,Yuying Li,Chengfu Zhang,Huali Zhang,Jing Zhao,Dong Pei,Tingfu Jiang,Lichun Zhao,Qingli Qu

The therapeutic potential of Olea europaea L. leaf in hepatitis is recognized, yet its active constituents against metabolic dysfunction-associated steatohepatitis (MASH), a specific form of hepatitis driven by metabolic disturbances, remain poorly defined. This study integrated HPLC fingerprinting of Olea europaea L. leaf extracts (OLE) with chemometrics and bioactivity profiling to identify anti-MASH components. Bioactivity was assessed using a palmitic acid-induced steatohepatitis model in L02 cells. Spectrum–effect relationships derived from pearson correlation and partial least squares regression highlighted four putative active compounds, designated P7, P8, P10, and P11. HPLC-MS identified these as cynaroside (P7), apigenin-7-O-glucoside (P8), oleuroside (P10), and ligustroside (P11). Subsequent in vitro and in vivo evaluations in a zebrafish MASH model confirmed that P7, P8, and P10 exhibited significant anti-MASH activity. Notably, a robust synergism was observed between cynaroside and oleuroside, which their 1:1 M combination yielded a ZIP synergy score of 11.965 and a combination index (CI) of 0.3151, indicating strong synergy at lower doses. These results identify key anti-MASH constituents in OLE and provide a mechanistic basis for using multi-component OLE, highlighting a synergistic approach for MASH management.

CAS / MDL: 57-10-3
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Food Bioscience · 2023 · IF 5.2

Curcumin alleviates lipid deposition in hepatocytes through miR-3666/AMPK axis regulation

Hengju Ge,Jiaxin Li,Yang Xu,Jiahong Xie,Naymul Karim,Fujie Yan,Jianling Mo,Wei Chen

Curcumin (CUR), the main compound extracted from Curcuma longa , has various biological actions, including hepatoprotective, anti-infective, anti-inflammatory, antioxidant, and neurotrophic properties. But it has not yet been clarified how CUR affects the accumulation of fatty in hepatic cells. Our study uncovered that CUR decreased the lipid deposition in free fat acids (FFAs)-treated hepatocytes, which could be blocked by Compound C (an AMPK inhibitor). This result suggests that protective effect was associated with the AMPK pathway activation. MiR-3666 directly targets the AMPK gene, and overexpression of miR-3666 greatly weakens the hypolipidemic effect of CUR. Our results showed that CUR reduced FFAs-induced lipid deposition by targeting miR-3666. This boosted AMPK phosphorylation and inhibited its downstream targets, including ACC and SREBP1 . These findings together confirm that CUR-mediated inhibition of miR-3666 to activate the AMPK pathway is a potential alternative for alleviation of hepatic lipid deposition.

研究领域: 药理学 · 分子生物学 · 肝病学
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