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1.
Nutrients ; 14(19)2022 Sep 29.
Article in English | MEDLINE | ID: mdl-36235710

ABSTRACT

A maternal low-protein (LP) diet during gestation and/or lactation results in metabolic syndrome in their offspring. Here, we investigated the effect of maternal LP diet during puberty and adulthood on the metabolic homeostasis of glucose and lipids in offspring. Female mice were fed with normal-protein (NP) diet or a LP diet for 11 weeks. Male offspring were then fed with a high-fat diet (NP-HFD and LP-HFD groups) or standard chow diet (NP-Chow and LP-Chow groups) for 4 months. Results showed that maternal LP diet during puberty and adulthood did not alter the insulin sensitivity and hepatic lipid homeostasis of their offspring under chow diet, but aggravated insulin resistance, hepatic steatosis, and hypercholesterolemia of offspring in response to a post-weaning HFD. Accordingly, transcriptomics study with offspring's liver indicated that several genes related to glucose and lipid metabolism, including lipoprotein lipase (Lpl), long-chain acyl-CoA synthetase 1 (Acsl1), Apoprotein A1 (Apoa1), major urinary protein 19 (Mup19), cholesterol 7α hydroxylase (Cyp7a1) and fibroblast growth factor 1 (Fgf1), were changed by maternal LP diet. Taken together, maternal LP diet during puberty and adulthood could disarrange the expression of metabolic genes in the liver of offspring and aggravate insulin resistance and hepatic steatosis in offspring fed a HFD.


Subject(s)
Fatty Liver , Insulin Resistance , Prenatal Exposure Delayed Effects , Animals , Apoproteins/metabolism , Cholesterol 7-alpha-Hydroxylase/metabolism , Coenzyme A/metabolism , Diet, High-Fat/adverse effects , Diet, Protein-Restricted/adverse effects , Fatty Liver/metabolism , Female , Fibroblast Growth Factor 1/metabolism , Glucose/metabolism , Ligases/metabolism , Lipid Metabolism/physiology , Lipids , Lipoprotein Lipase/metabolism , Liver/metabolism , Male , Maternal Nutritional Physiological Phenomena , Mice , Pregnancy , Prenatal Exposure Delayed Effects/metabolism , Sexual Maturation
2.
JACC Basic Transl Sci ; 7(8): 820-840, 2022 Aug.
Article in English | MEDLINE | ID: mdl-36061341

ABSTRACT

Chronic kidney disease (CKD) is well recognized as a distinct contributor to cardiac hypertrophy, while the underlying mechanism remains incompletely understood. Here, the authors show that myocardial mitochondrial oxidative damage is early and prominent in CKD and distinctively stimulates the STING-NFκB pathway by releasing mitochondrial DNA to drive cardiac hypertrophy. Furthermore, the authors reveal that ornithine decarboxylase (ODC1)-putrescine metabolic flux is transactivated by NFκB and is required for the STING-NFκB pathway to drive cardiac hypertrophy. Finally, genetic or pharmacologic inhibition of the myocardial mitochondria-STING-NFκB-ODC1 axis significantly prevents CKD-associated cardiac hypertrophy. Therefore, targeting the myocardial mitochoandria-STING-NFκB-ODC1 axis is a promising therapeutic strategy for cardiac hypertrophy in patients with CKD.

3.
Oxid Med Cell Longev ; 2022: 8006642, 2022.
Article in English | MEDLINE | ID: mdl-36120595

ABSTRACT

Atherosclerosis is the key pathogenesis of cardiovascular diseases; oxidative stress, which is induced by the generated excess reactive oxygen species (ROS), has been a crucial mechanism underlying this pathology. Nanoparticles (NPs) represent a novel strategy for the development of potential therapies against atherosclerosis, and multifunctional NPs possessing antioxidative capacities hold promise for amelioration of vascular injury caused by ROS and for evading off-target effects; materials that are currently used for NP synthesis often serve as vehicles that do not possess intrinsic biological activities; however, they may affect the surrounding healthy environment due to decomposition of products. Herein, we used nontoxic fucoidan, a sulfated polysaccharide derived from a marine organism, to develop chitosan-fucoidan nanoparticles (CFNs). Then, by binding to P-selectin, an inflammatory adhesion exhibited molecule expression on the endothelial cells and activated platelets, blocking leukocyte recruitment and rolling on platelets and endothelium. CFNs exhibit antioxidant and anti-inflammatory properties. Nevertheless, by now, the application of CFNs for the target delivery regarding therapeutics specific to atherosclerotic plaques is not well investigated. The produced CFNs were physicochemically characterized using transmission electron microscopy (TEM), together with Fourier transform infrared spectroscopy (FTIR). Evaluations of the in vitro antioxidant as well as anti-inflammatory activities exhibited by CFNs were based on the measurement of their ROS scavenging abilities and investigating inflammatory mediator levels. The in vivo pharmacokinetics and binding efficiency of the CFNs to atherosclerotic plaques were also evaluated. The therapeutic effects indicated that CFNs effectively suppressed local oxidative stress and inflammation by targeting P-selectin in atheromatous plaques and thereby preventing the progression of atherosclerosis.


Subject(s)
Atherosclerosis , Chitosan , Nanoparticles , Plaque, Atherosclerotic , Antioxidants/chemistry , Antioxidants/pharmacology , Antioxidants/therapeutic use , Atherosclerosis/drug therapy , Atherosclerosis/metabolism , Chitosan/therapeutic use , Endothelial Cells/metabolism , Humans , Inflammation Mediators , Nanoparticles/chemistry , P-Selectin , Polysaccharides/chemistry , Polysaccharides/pharmacology , Polysaccharides/therapeutic use , Reactive Oxygen Species/metabolism
4.
Theranostics ; 12(11): 5069-5085, 2022.
Article in English | MEDLINE | ID: mdl-35836796

ABSTRACT

Rationale: Acute kidney injury (AKI) is pathologically characterized by renal tubular epithelial cell (RTEC) death and interstitial inflammation, while their pathogenesis remains incompletely understood. Dual-specificity phosphatase 2 (DUSP2) recently emerges as a crucial regulator of cell death and inflammation in a wide range of diseases, but its roles in renal pathophysiology are largely unknown. Methods: The expression of DUSP2 in the kidney was characterized by histological analysis in renal tissues from patients and mice with AKI. The role and mechanism of DUSP2-mediated inhibition of tubular epithelial cell pyroptosis in AKI were evaluated both in vivo and in vitro, and confirmed in RTEC-specific deletion of DUSP2 mice. Results: Here, we show that DUSP2 is enriched in RTECs in the renal tissue of both human and mouse and mainly positions in the nucleus. Further, we reveal that loss-of-DUSP2 in RTECs not only is a common feature of human and murine AKI but also positively contributes to AKI pathogenesis. Especially, RTEC-specific deletion of DUSP2 sensitizes mice to AKI by promoting RTEC pyroptosis and the resultant interstitial inflammation. Mechanistic studies show that gasdermin D (GSDMD), which mediates RTEC pyroptosis, is identified as a transcriptional target of activated STAT1 during AKI, whereas DUSP2 as a nuclear phosphatase deactivates STAT1 to restrict GSDMD-mediated RTEC pyroptosis. Importantly, DUSP2 overexpression in RTECs via adeno-associated virus-mediated gene transfer significantly ameliorates AKI. Conclusion: Our findings demonstrate a hitherto unrecognized role of DUSP2-STAT1 axis in regulating RTEC pyroptosis in AKI, highlighting that DUSP2-STAT1 axis is an attractive therapeutic target for AKI.


Subject(s)
Acute Kidney Injury , Pyroptosis , Acute Kidney Injury/metabolism , Animals , Dual Specificity Phosphatase 2/metabolism , Epithelial Cells/metabolism , Humans , Inflammation/metabolism , Mice , Mice, Inbred C57BL , Pyroptosis/physiology
5.
Cell Rep ; 38(7): 110392, 2022 02 15.
Article in English | MEDLINE | ID: mdl-35172146

ABSTRACT

The composition and origin of extrinsic cues required for hematopoietic stem cell (HSC) maintenance are incompletely understood. Here we identify renal Klotho and inorganic phosphate (Pi) as extrinsic factors that antagonistically regulate HSC maintenance in the bone marrow (BM). Disruption of the Klotho-Pi axis by renal Klotho deficiency or Pi excess causes Pi overload in the BM niche and Pi retention in HSCs, leading to alteration of HSC maintenance. Mechanistically, Pi retention is mediated by soluble carrier family 20 member 1 (SLC20A1) and sensed by diphosphoinositol pentakisphosphate kinase 2 (PPIP5K2) to enhance Akt activation, which then upregulates SLC20A1 to aggravate Pi retention and augments GATA2 activity to drive the expansion and megakaryocyte/myeloid-biased differentiation of HSCs. However, kidney-secreted soluble Klotho directly maintains HSC pool size and differentiation by restraining SLC20A1-mediated Pi absorption of HSCs. These findings uncover a regulatory role of the Klotho-Pi axis orchestrated by the kidneys in BM HSC maintenance.


Subject(s)
Hematopoietic Stem Cells/cytology , Kidney/metabolism , Klotho Proteins/metabolism , Phosphates/metabolism , Animals , Bone Marrow Cells/metabolism , Cell Differentiation , GATA2 Transcription Factor/metabolism , Hematopoietic Stem Cells/metabolism , Homeostasis , Klotho Proteins/deficiency , Mice, Inbred C57BL , Phosphotransferases (Phosphate Group Acceptor)/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Sodium-Phosphate Cotransporter Proteins, Type III/metabolism , Solubility
6.
Adv Sci (Weinh) ; 8(5): 2002738, 2021 Mar.
Article in English | MEDLINE | ID: mdl-33717842

ABSTRACT

Chronic kidney disease (CKD) is associated with accelerated atherosclerosis progression and high incidence of cardiovascular events, hinting that atherosclerotic plaques in CKD may be vulnerable. However, its cause and mechanism remain obscure. Here, it is shown that apolipoprotein E-deficient (ApoE-/-) mouse with CKD (CKD/ApoE-/- mouse) is a useful model for investigating the pathogenesis of plaque vulnerability, and premature senescence and phenotypic switching of vascular smooth muscle cells (VSMCs) contributes to CKD-associated plaque vulnerability. Subsequently, VSMC phenotypes in patients with CKD and CKD/ApoE-/- mice are comprehensively investigated. Using multi-omics analysis and targeted and VSMC-specific gene knockout mice, VSMCs are identified as both type-I-interferon (IFN-I)-responsive and IFN-I-productive cells. Mechanistically, mitochondrial damage resulting from CKD-induced oxidative stress primes the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway to trigger IFN-I response in VSMCs. Enhanced IFN-I response then induces VSMC premature senescence and phenotypic switching in an autocrine/paracrine manner, resulting in the loss of fibrous cap VSMCs and fibrous cap thinning. Conversely, blocking IFN-I response remarkably attenuates CKD-associated plaque vulnerability. These findings reveal that IFN-I response in VSMCs through immune sensing of mitochondrial damage is essential for the pathogenesis of CKD-associated plaque vulnerability. Mitigating IFN-I response may hold promise for the treatment of CKD-associated cardiovascular diseases.

7.
Adipocyte ; 9(1): 523-534, 2020 12.
Article in English | MEDLINE | ID: mdl-32876525

ABSTRACT

Adipose tissue inflammation plays an important role in the regulation of glucose and lipids metabolism. It is unknown whether Ursolic acid (UA) could regulate adipose tissue inflammation, though it can regulate inflammation in many other tissues. In this study, 3T3-L1 adipocytes, DIO mice and lean mice were treated with UA or vehicle. Gene expression of inflammatory factors, chemokines and immune markers in adipocytes and adipose tissue, cytokines in cell culture medium and serum, and inflammation regulatory pathways in adipocytes were detected. Results showed that UA increased the expression of interleukins and chemokines, but not TNFα, in both adipocytes and adipose tissue. IL6 and MCP1 levels in the cell culture medium and mouse serum were induced by UA treatment. Cd14 expression level and number of CD14+ monocytes were higher in UA treated adipose tissue than those in the control group. Glucose tolerance test was impaired by UA treatment in DIO mice. Mechanistically, UA induced the expression of Tlr4 and the phosphorylation levels of ERK and NFκB in adipocytes. In conclusion, our study indicated that short-term UA administration could induce CD14+ monocytes infiltration by increasing the production of interleukins and chemokines in mouse adipose tissue, which might further impair glucose tolerance test.


Subject(s)
Adipocytes/drug effects , Adipocytes/metabolism , Adipose Tissue/metabolism , Chemokines/biosynthesis , Interleukin-6/biosynthesis , Triterpenes/pharmacology , 3T3-L1 Cells , Animals , Biomarkers , Chemokines/genetics , Cytokines/biosynthesis , Cytokines/genetics , Female , Gene Expression Regulation/drug effects , Inflammation Mediators/metabolism , Lipogenesis/drug effects , Lipogenesis/genetics , Male , Mice , Monocytes/drug effects , Monocytes/metabolism , Phosphorylation , Signal Transduction/drug effects , Ursolic Acid
8.
Front Plant Sci ; 11: 749, 2020.
Article in English | MEDLINE | ID: mdl-32595669

ABSTRACT

In land plants, the pentatricopeptide repeat (PPR) proteins form a large family involved in post-transcriptional processing of RNA in mitochondria and chloroplasts, which is critical for plant development and evolutionary adaption. Although studies showed a number of PPR proteins generally influence the editing of organellar genes, few of them were characterized in detail in rice. Here, we report a PLS-E subclass PPR protein in rice, PPR756, loss of function of which led to the abolishment of RNA editing events among three mitochondrial genes including atp6, ccmC, and nad7. Their defective C-to-U transformation then resulted in improper amino acid retention which could cause abortive pollen development. Furthermore, PPR756 could bind to the three target genes directly and interact with three OsMORFs (multiple organellar RNA editing factors): OsMORF1, OsMORF8-1, and OsMORF8-2. The knock-out plants of PPR756 exhibited retarded growth and greener leaves during the early vegetative stages, along with sterile pollen and lower seed setting at the reproductive stage. These results established a role for PPR756 in rice development, participating in RNA editing of three various transcripts and cooperating with OsMORFs via an editosome manner in rice.

9.
Biochem Biophys Res Commun ; 515(4): 614-620, 2019 08 06.
Article in English | MEDLINE | ID: mdl-31176485

ABSTRACT

Hexokinases (HXKs) have determined to be multifaceted proteins, and they are the only ones able to phosphorylate glucose in plants. However, the binding mode for ATP to plant HXKs remains unclear. Here, we report the crystal structures of rice hexokinase 6 (OsHXK6) in four different forms: (i) apo-form, (ii) binary complex with D-Glc, (iii) quaternary complex with ADP, PO4 and Mg2+, and (iv) pentanary complex with D-Glc, ADP, PO4, and Mg2+. The apo form is in the open state conformation, and the three others are in the closed state, indicating that glucose and ADP-PO4 binding induces a large conformational change by domain rearrangement. The quaternary complex is a novel intermediate during the catalytic reaction we trapped for the first time, which provides a new evidence for the enzymatic mechanism of HXKs. In addition, the latter two complexes reveal the binding mode for ADP-PO4 to plant HXKs, which provide the structural explanation for the dual-function of OsHXK6. In addition, we identified that residues Gly112, Thr261, Gly262, and Gly450 are essential to the binding between ADP-PO4 and OsHXK6 by a series of single mutations and enzymatic assays. Our study provide structural basis for the other functional studies of OsHXK6 in rice.


Subject(s)
Crystallography, X-Ray , Hexokinase/chemistry , Oryza/enzymology , Plant Proteins/chemistry , Adenosine Triphosphate/chemistry , Binding Sites , Catalysis , Codon , Glucose/chemistry , Hydrolysis , Magnesium/chemistry , Mutagenesis, Site-Directed , Mutation , Oryza/genetics , Phosphorylation , Protein Binding , Protein Domains , Protein Structure, Quaternary , Signal Transduction , Substrate Specificity
10.
EBioMedicine ; 41: 623-635, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30772303

ABSTRACT

BACKGROUND: Global consumption of protein per capita is rising, while rates of infertility are increasing. However, a clear relationship between protein intake and reproductive health has not been demonstrated. The activation of the quiescent primordial follicles is the first step of folliculogenesis, and their activation must be tightly controlled to prevent premature exhaustion of the ovarian follicular reserve. METHODS: The primordial follicle reserve of wild-type or liver-specific ablation of fibroblast growth factor 21 (FGF21) in mice, subjected to limited or excessive protein diets or oral gavage test, were detected in vivo. Mouse ovary organ cultures were used to examine the direct role of metabolites or metabolic hormones on primordial follicle activation. FINDINGS: Mouse primordial follicle activation, was reduced by restricted protein intake and was accelerated by excessive protein intake, in an ovarian mTORC1 signaling-dependent manner. Furthermore, restricted or excessive protein intake resulted in an augmentation or decline of oocyte number and fertility at older age, respectively. Liver-specific ablation of FGF21, which resulted in a reduction of 87% in circulating FGF21, abrogated the preserving effect of low-protein intake on primordial follicle pool. Interestingly, FGF21 had no direct effect on the activation of primordial follicles, but instead required an adipokine adiponectin. Moreover, AdipoRon, an oral adiponectin receptor agonist, prevented the over-activation effect of excessive protein intake on primordial follicle activation. INTERPRETATION: Dietary protein consumption controlled ovarian primordial follicle reserve and fertility, which required coordination between FGF21 and adiponectin. FUND: Natural Science Foundation of China (Grant 31772616).


Subject(s)
Adiponectin/metabolism , Diet, Protein-Restricted , Fibroblast Growth Factors/genetics , Adiponectin/blood , Administration, Oral , Animals , Female , Fibroblast Growth Factors/blood , Fibroblast Growth Factors/metabolism , In Vitro Techniques , Liver/metabolism , Mechanistic Target of Rapamycin Complex 1/metabolism , Mice , Mice, Inbred C57BL , Oocytes/cytology , Organ Culture Techniques , Ovarian Follicle/drug effects , Ovarian Follicle/growth & development , Ovarian Follicle/metabolism , Ovary/metabolism , Ovary/pathology , Piperidines/pharmacology , RNA, Messenger/metabolism , Signal Transduction
11.
Plant Biotechnol J ; 17(5): 906-913, 2019 05.
Article in English | MEDLINE | ID: mdl-30321482

ABSTRACT

Marker-based prediction holds great promise for improving current plant and animal breeding efficiencies. However, the predictabilities of complex traits are always severely affected by negative factors, including distant relatedness, environmental discrepancies, unknown population structures, and indeterminate numbers of predictive variables. In this study, we utilised two independent F1 hybrid populations in the years 2012 and 2015 to predict rice thousand grain weight (TGW) using parental untargeted metabolite profiles with a partial least squares regression method. A stable predictive model for TGW was built based on hybrids from the population in 2012 (r = 0.75) but failed to properly predict TGW for hybrids from the population in 2015 (r = 0.27). After integrating hybrids from both populations into the training set, the TGW of hybrids could be predicted but was largely dependent on population structures. Then, core hybrids from each population were determined by principal component analysis and the TGW of hybrids in both environments were successfully predicted (r > 0.60). Moreover, adjusting the population structures and numbers of predictive analytes increased TGW predictability for hybrids in 2015 (r = 0.72). Our study demonstrates that the TGW of F1 hybrids across environments can be accurately predicted based on parental untargeted metabolite profiles with a core hybridisation strategy in rice. Metabolic biomarkers identified from early developmental stage tissues, which are grown under experimental conditions, may represent a workable approach towards the robust prediction of major agronomic traits for climate-adaptive varieties.


Subject(s)
Edible Grain/growth & development , Metabolome , Oryza/growth & development , Biomarkers , Edible Grain/metabolism , Environment , Hybridization, Genetic , Least-Squares Analysis , Oryza/metabolism , Plant Breeding
12.
New Phytol ; 220(3): 878-892, 2018 11.
Article in English | MEDLINE | ID: mdl-30019754

ABSTRACT

The pentatricopeptide repeat (PPR) protein family is a large family characterized by tandem arrays of a degenerate 35-amino-acid motif whose members function as important regulators of organelle gene expression at the post-transcriptional level. Despite the roles of PPRs in RNA editing in organelles, their editing activities and the underlying mechanism remain obscure. Here, we show that a novel DYW motif-containing PPR protein, PPS1, is associated with five conserved RNA-editing sites of nad3 located in close proximity to each other in mitochondria, all of which involve conversion from proline to leucine in rice. Both pps1 RNAi and heterozygous plants are characterized by delayed development and partial pollen sterility at vegetative stages and reproductive stage. RNA electrophoresis mobility shift assays (REMSAs) and reciprocal competition assays using different versions of nad3 probes confirm that PPS1 can bind to cis-elements near the five affected sites, which is distinct from the existing mode of PPR-RNA binding because of the continuity of the editing sites. Loss of editing at nad3 in pps1 reduces the activity of several complexes in the mitochondrial electron transport chain and affects mitochondrial morphology. Taken together, our results indicate that PPS1 is required for specific editing sites in nad3 in rice.


Subject(s)
Mitochondria/metabolism , Oryza/genetics , Plant Proteins/chemistry , Plant Proteins/metabolism , RNA Editing/genetics , Amino Acid Motifs , Base Sequence , Cell Nucleus/metabolism , Conserved Sequence , Electron Transport , Evolution, Molecular , Gene Expression Regulation, Plant , Mitochondria/ultrastructure , Mitochondrial Proteins/chemistry , Mitochondrial Proteins/metabolism , Oryza/ultrastructure , Phenotype , Pollen/metabolism , Pollen/ultrastructure , Protein Binding , RNA Interference , RNA, Messenger/genetics , RNA, Messenger/metabolism , Time Factors
13.
FASEB J ; 32(10): 5602-5611, 2018 10.
Article in English | MEDLINE | ID: mdl-29718710

ABSTRACT

Both ovarian E2 and hepatic fibroblast growth factor 21 (FGF21) are critical for energy homeostasis and white adipose tissue browning. Estrogen receptor α (ERα) is abundantly expressed in liver. However, whether FGF21 has a role in E2-induced white adipose tissue browning remains uncertain. In this study, we showed that hepatic Fgf21 expression and secretion during estrus cycle changed with the tetradian oscillatory secretion of circulation E2 in adult, female mice, with their peak expressions and secretions at the proestrus. In addition, exogenous E2 robustly stimulated liver Fgf21 expression and elevated serum FGF21 concentrations, which induced browning gene expression and reduced the tissue weight in subcutaneous white adipose in mice with ovariectomies. The inhibitor of mammalian target of rapamycin (mTOR) and of ERα blocked the induction effect of E2 on the expression of Fgf21 in primary hepatocytes, which revealed that E2 might stimulate FGF21 expression via the ERα-mTOR pathway. Furthermore, FGF21 liver-specific deficiency abolished E2-induced white adipose browning in mice with ovariectomies. This study indicates that ovarian E2 increased liver FGF21 expression directly, which in turn, functioned as an endocrine signal to influence inguinal white adipose tissue browning.-Hua, L., Zhuo, Y., Jiang, D., Li, J., Huang, X., Zhu, Y., Li, Z., Yan, L., Jin, C., Jiang, X., Che, L., Fang, Z., Lin, Y., Xu, S., Li, J., Feng, B., Wu, D. Identification of hepatic fibroblast growth factor 21 as a mediator in 17ß-estradiol-induced white adipose tissue browning.


Subject(s)
Adipose Tissue, Brown/metabolism , Adipose Tissue, White/metabolism , Estradiol/pharmacology , Fibroblast Growth Factors/biosynthesis , Gene Expression Regulation/drug effects , Hepatocytes/metabolism , Adipose Tissue, Brown/cytology , Adipose Tissue, White/cytology , Animals , Estrogen Receptor alpha/agonists , Estrogen Receptor alpha/genetics , Estrogen Receptor alpha/metabolism , Female , Fibroblast Growth Factors/genetics , Hepatocytes/cytology , Mice , Mice, Knockout , TOR Serine-Threonine Kinases/metabolism
14.
J Exp Bot ; 69(12): 2923-2936, 2018 05 25.
Article in English | MEDLINE | ID: mdl-29562289

ABSTRACT

In flowering plants, various RNA editing events occur in the mitochondria and chloroplasts as part of post-transcriptional processes. Although several pentatricopeptide repeat (PPR) proteins and multiple organellar RNA editing factors (MORFs) have been identified as RNA editing factors, the underlying mechanism of PPRs and the cooperation among these proteins are still obscure. Here, we identified a rice dual-localized PPR protein, OsPGL1. The loss of function of OsPGL1 resulted in defects in both chloroplast RNA editing of ndhD-878 and mitochondrial RNA editing of ccmFc-543, both of which could be restored in transgenic complementation lines. Despite synonymous editing of ccmFc-543, the loss of editing of ndhD-878 caused a failed conversion of serine to leucine, leading to chloroplast dysfunction and defects in the photosynthetic complex; the results of additional experiments demonstrated that OsPGL1 directly binds to both transcripts. Interactions between three OsMORFs (OsMORF2/8/9) and OsPGL1 both in vitro and in vivo were confirmed, implying that OsPGL1 functions in RNA editing via an editosome. These findings also suggested that OsMORFs assist with and contribute to a flexible PPR-RNA recognition model during RNA editing. These results indicate that, in cooperation with PPRs, OsPGL1 is required for RNA editing. In addition, our study provides new insights into the relationship between RNA editing and plant development.


Subject(s)
Chloroplasts/metabolism , Mitochondria/metabolism , Oryza/genetics , Plant Proteins/genetics , RNA Editing , Amino Acid Sequence , Oryza/metabolism , Plant Proteins/metabolism , Sequence Alignment
15.
Nutrients ; 9(10)2017 Oct 18.
Article in English | MEDLINE | ID: mdl-29057818

ABSTRACT

The trace element zinc plays an important role in human life. Zinc deficiency impairs growth, reproduction, metabolism and immunity in both human and animals. Thus, zinc supplementation is recommended in daily life. However, the effect of long-term chronic zinc supplementation on adipose homeostasis has not been well elucidated. In the current study, mice were supplemented with zinc sulfate in the drinking water for 20 weeks. The results suggested that chronic zinc supplementation impaired systemic glucose clearance after exogenous insulin or glucose challenges, as compared to the control mice. Further study revealed that chronic zinc supplementation made no difference to body weight, but increased visceral adipose tissue weight and adipocyte size. In addition, gene expression of leptin and IL6 in the visceral adipose tissue of zinc-supplemented mice were higher than those of control mice. Moreover, serum level of leptin of the zinc-supplemented mice was twice as high as that of the control mice. Besides, phosphorylation level of AKT T308 was attenuated in the perirenal adipose tissue of zinc-supplemented mice. In comparison, the expression of macrophage marker genes and lipogenic genes were not affected by chronic zinc supplementation, but the protein levels of FAS and SCD1 decreased or tended to decrease in the perirenal adipose tissue of zinc-supplemented mice, as compared to the control mice. Our findings suggest that chronic high dose zinc supplementation induces visceral adipose tissue hypertrophy and impairs AKT signaling in perirenal adipose tissue.


Subject(s)
Adiposity/drug effects , Dietary Supplements/toxicity , Intra-Abdominal Fat/drug effects , Zinc Sulfate/toxicity , 3T3-L1 Cells , Adipocytes/drug effects , Adipocytes/metabolism , Adipocytes/pathology , Animals , Blood Glucose/metabolism , Cell Size/drug effects , Drug Administration Schedule , Hypertrophy , Interleukin-6/genetics , Interleukin-6/metabolism , Intra-Abdominal Fat/metabolism , Intra-Abdominal Fat/pathology , Intra-Abdominal Fat/physiopathology , Leptin/genetics , Leptin/metabolism , Lipids/blood , Male , Mice , Mice, Inbred C57BL , Phosphorylation , Proto-Oncogene Proteins c-akt/metabolism , Stearoyl-CoA Desaturase/metabolism , Time Factors , Zinc Sulfate/administration & dosage , fas Receptor/metabolism
16.
Carbohydr Polym ; 174: 915-922, 2017 Oct 15.
Article in English | MEDLINE | ID: mdl-28821148

ABSTRACT

The extensive prospects of polysaccharides in medicine and pharmaceuticals have elicited much interest. Ligusticum chuanxiong polysaccharides, previously extracted as neutral polysaccharides, exhibit antioxidant, anticancer, andantibacterial capacities in vitro. Here we show one pectic polysaccharide extracted from rhizome of L. chuanxiong(LCP-II-I). Structural analysis indicated its long homogalacturonan region is interrupted by rhamnogalacturonan type I, with arabinan and arabinogalactan type I as side chains. Intake of the LCP-II-I significantly promoted the expression of antioxidant enzymes and their master regulator PGC-1α, resulting in higher antioxidant capacity in jejunum and cecum of aged mice. Consistently, treatment with LCP-II-I promotes antioxidant enzymes expression, and protects SW480 cells against H2O2 induced oxidative stress. Our work isolates and identifies a pectic polysaccharide, LCP-II-I, and reveals its potential application in antioxidant defense, which will be important for oxidative stress related disorders treatment in aging intestine.


Subject(s)
Antioxidants/metabolism , Intestines/drug effects , Ligusticum/chemistry , Pectins/pharmacology , Aging , Animals , Cell Line , Hydrogen Peroxide , Intestinal Mucosa/metabolism , Male , Mice , Mice, Inbred C57BL , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Polysaccharides , Rhizome/chemistry
17.
Methods Mol Biol ; 1640: 211-217, 2017.
Article in English | MEDLINE | ID: mdl-28608345

ABSTRACT

Small noncoding RNAs are essential for gene expression at transcriptional and posttranscriptional levels. Northern blot is the most used method for small RNA detection in tissues. Here we present an improved protocol for the Northern blot-based small RNA detection from plant tissues by using biotin-labeled probes. MicroRNAs and small interfering RNAs derived from Arabidopsis and Oryza sativa, respectively, have been detected with this methodology. Results suggest that this method is sensitive and efficient enough to detect small RNAs from plant tissues by using as low as 5 µg of total RNA. Furthermore, biotin-labeled probes are safer and easier to store for long term than radiolabeled probes.


Subject(s)
Arabidopsis/chemistry , Blotting, Northern/methods , Nucleic Acid Hybridization/methods , Oryza/chemistry , RNA, Plant/analysis , RNA, Small Untranslated/analysis , Arabidopsis/genetics , Biotin/chemistry , Oligonucleotide Probes/chemistry , Oryza/genetics , RNA, Plant/genetics , RNA, Small Untranslated/genetics
18.
Front Plant Sci ; 8: 986, 2017.
Article in English | MEDLINE | ID: mdl-28638401

ABSTRACT

Hybrid rice has contributed significantly to the world food security. Breeding of elite high-yield, strong-resistant broad-spectrum restorer line is an important strategy for hybrid rice in commercial breeding programs. Here, we developed three elite brown planthopper (BPH)-resistant wide-spectrum restorer lines by pyramiding big-panicle gene Gn8.1, BPH-resistant genes Bph6 and Bph9, fertility restorer genes Rf3, Rf4, Rf5, and Rf6 through molecular marker assisted selection. Resistance analysis revealed that the newly developed restorer lines showed stronger BPH-resistance than any of the single-gene donor parent Luoyang-6 and Luoyang-9. Moreover, the three new restorer lines had broad spectrum recovery capabilities for Honglian CMS, Wild abortive CMS and two-line GMS sterile lines, and higher grain yields than that of the recurrent parent 9,311 under nature field conditions. Importantly, the hybrid crosses also showed good performance for grain yield and BPH-resistance. Thus, the development of elite BPH-resistant wide-spectrum restorer lines has a promising future for breeding of broad spectrum BPH-resistant high-yield varieties.

19.
Plant Cell Environ ; 39(12): 2740-2753, 2016 12.
Article in English | MEDLINE | ID: mdl-27627618

ABSTRACT

The drought-induced 19 protein family consists of several atypical Cys2/His2-type zinc finger proteins in plants and plays an important role in abiotic stress. In this study, we found that overexpressing OsDi19-4 in rice altered the expression of a series of abscisic acid (ABA)-responsive genes, resulting in strong ABA-hypersensitive phenotypes including ABA-induced seed germination inhibition, early seedling growth inhibition and stomatal closure. On the contrary, OsDi19-4 knockdown lines were less sensitive to ABA. Additionally, OsCDPK14 was identified to interact with OsDi19-4 and be responsible for the phosphorylation of OsDi19-4, and the phosphorylation of OsDi19-4 was further enhanced after the treatment of ABA. Apart from these, OsDi19-4 was shown to directly bind to the promoters of OsASPG1 and OsNAC18 genes, two ABA-responsive genes, and regulate their expression. Transient expression assays confirmed the direct regulation role of OsDi19-4, and the regulation was further enhanced by the increased phosphorylation of OsDi19-4 after the treatment of ABA. Taken together, these data demonstrate that OsDi19-4 acts downstream of OsCDPK14 to positively regulate ABA response by modulating the expression of ABA-responsive genes in rice.


Subject(s)
Abscisic Acid/physiology , Oryza/physiology , Plant Growth Regulators/physiology , Plant Proteins/physiology , Abscisic Acid/metabolism , Gene Expression Regulation, Plant/physiology , Gene Knockdown Techniques , Germination , Immunoprecipitation , Oryza/metabolism , Plant Growth Regulators/metabolism , Plant Proteins/metabolism , Real-Time Polymerase Chain Reaction , Seeds/physiology , Transcription Factors/physiology , Two-Hybrid System Techniques , Zinc Fingers/physiology
20.
G3 (Bethesda) ; 6(6): 1491-502, 2016 06 01.
Article in English | MEDLINE | ID: mdl-27172200

ABSTRACT

Semidwarfism is an important agronomic trait in rice breeding programs. The semidwarf mutant gene Sdt97 was previously described. However, the molecular mechanism underlying the mutant is yet to be elucidated. In this study, we identified the mutant gene by a map-based cloning method. Using a residual heterozygous line (RHL) population, Sdt97 was mapped to the long arm of chromosome 6 in the interval of nearly 60 kb between STS marker N6 and SNP marker N16 within the PAC clone P0453H04. Sequencing of the candidate genes in the target region revealed that a base transversion from G to C occurred in the 5' untranslated region of Sdt97 qRT-PCR results confirmed that the transversion induced an obvious change in the expression pattern of Sdt97 at different growth and developmental stages. Plants transgenic for Sdt97 resulted in the restoration of semidwarfism of the mutant phenotype, or displayed a greater dwarf phenotype than the mutant. Our results indicate that a point mutation in the 5' untranslated region of Sdt97 confers semidwarfism in rice. Functional analysis of Sdt97 will open a new field of study for rice semidwarfism, and also expand our knowledge of the molecular mechanism of semidwarfism in rice.


Subject(s)
5' Untranslated Regions , Genes, Plant , Oryza/genetics , Point Mutation , Quantitative Trait, Heritable , Base Sequence , Breeding , Chromosome Mapping , Cloning, Molecular , DNA Mutational Analysis , Gene Expression Regulation, Plant , Genetic Association Studies , Genotype , Phenotype , Plants, Genetically Modified , Polymorphism, Single Nucleotide
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