ABSTRACT
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease, and the intestinal flora and its metabolites play an important role in the amelioration of central nervous system (CNS) disorders such as AD through a bidirectional interaction between the gut-brain axis (GBA). Nicotinamide mononucleotide (NMN), one of the precursors for nicotinamide adenine dinucleotide (NAD+) synthesis, reduces the brain features of AD, including neuroinflammation, mitochondrial abnormalities, synaptic dysfunction, and cognitive impairment. However, the impact of NMN on the gut flora of AD is still unknown. In the current study, we investigated the relationship between gut flora and NMN treatment in APP/PS1 transgenic (AD) mice through the 16S ribosomal RNA (rRNA) high-throughput sequencing analysis of mouse feces after being treated with NMN for 16 weeks. The results show that the NMN significantly changed the intestinal microbial community composition in AD mice. The NMN also increased the relative abundance of short-chain fatty acids (SCFAs)-producing bacteria such as Lactobacillus and Bacteroides at the genus level by protecting intestinal health and improving AD. The overall results suggest novel therapeutic strategies for treating AD and highlight the critical role of gut microbiota in AD pathology, and layout the further research.
Subject(s)
Alzheimer Disease , Gastrointestinal Microbiome , Neurodegenerative Diseases , Mice , Animals , Alzheimer Disease/metabolism , Gastrointestinal Microbiome/physiology , Nicotinamide Mononucleotide/pharmacology , Nicotinamide Mononucleotide/metabolism , Nicotinamide Mononucleotide/therapeutic use , Neurodegenerative Diseases/metabolism , Brain/metabolismABSTRACT
The interplay among cigarette smoking status, oral microbiota, and cardiometabolic health is poorly understood. We aimed to examine the association of cigarette smoking status with oral microbiota and to assess the association of the identified microbial features with cardiometabolic risk factors in a Chinese population. This study included 587 participants within the Central China Cohort, including 111 smokers and 476 non-smokers, and their oral microbiota was profiled by 16S rRNA sequencing. Both oral microbial alpha- and beta-diversity were distinct between smokers and non-smokers (p < 0.05). With adjustment for sociodemographics, alcohol and tea drinking, tooth brushing frequency, and body mass index, the relative abundance of nine genera and 26 pathways, including the genus Megasphaera and two pathways involved in inositol degradation which have potentially adverse effects on cardiometabolic health, was significantly different between two groups (FDR q < 0.20). Multiple microbial features related to cigarette smoking were found to partly mediate the associations of cigarette smoking with serum triglycerides and C-reactive protein levels (p-mediation < 0.05). In conclusion, cigarette smoking status may have impacts on the oral microbial features, which may partially mediate the associations of cigarette smoking and cardiometabolic health.
Subject(s)
Cardiovascular Diseases , Cigarette Smoking , Microbiota , Mouth , Adult , Humans , Bacteria/genetics , Cardiovascular Diseases/epidemiology , Cigarette Smoking/adverse effects , East Asian People , RNA, Ribosomal, 16S/genetics , Mouth/microbiologyABSTRACT
Plants cannot avoid environmental challenges and are constantly threatened by diverse biotic and abiotic stresses. However, plants have developed a unique immune system to defend themselves against the invasion of various pathogens. Melatonin, N-acetyl-5-methoxytryptamine has positive physiological effects in plants that are involved in disease resistance. The processes underlying melatonin-induced pathogen resistance in plants are still unknown. The current study explores how melatonin regulates the plant-disease interaction in maize. The results showed that 400 µM melatonin strongly reduced the disease lesion on maize stalks by 1.5 cm and corn by 4.0 cm caused by Fusarium graminearum PH-1. Furthermore, after treatment with melatonin, the plant defense enzymes like SOD significantly increased, while POD and APX significantly decreased compared to the control. In addition, melatonin can also improve maize's innate immunity, which is mediated by melatonin treatments through the salicylic acid signaling pathway, and up-regulate the defense-associated expression of PR1, LOX1, OXR, serPIN, and WIPI genes in maize. Melatonin not only inhibits the disease in the maize stalks and corn, but also down-regulates the deoxynivalenol (DON) production-related expression of genes Tri1, Tri4, Tri5, and Tri6 in maize. Overall, this study sheds new light on the mechanisms by which melatonin regulates antioxidant enzymes and defense-related genes involved in plant immunity to effectively suppress plant diseases.
Subject(s)
Fusarium , Melatonin , Melatonin/pharmacology , Zea mays/metabolism , Virulence , Plants , Plant DiseasesABSTRACT
Root systems anchor plants to the substrate in addition to transporting water and nutrients, playing a fundamental role in plant survival. The LAZY1 gene mediates gravity signal transduction and participates in root and shoot development and auxin flow in many plants. In this study, a regulator, LsLAZY1, was identified from Leymus secalinus based on previous transcriptome data. The conserved domain and evolutionary relationship were further analyzed comprehensively. The role of LsLAZY1 in root development was investigated by genetic transformation and associated gravity response and phototropism assay. Subcellular localization showed that LsLAZY1 was localized in the nucleus. LsLAZY1 overexpression in Arabidopsis thaliana (Col-0) increased the length of the primary roots (PRs) and the number of lateral roots (LRs) compared to Col-0. Furthermore, 35S:LsLAZY1 transgenic seedlings affected auxin transport and showed a stronger gravitational and phototropic responses. It also promoted auxin accumulation at the root tips. These results indicated that LsLAZY1 affects root development and auxin transport. Supplementary Information: The online version contains supplementary material available at 10.1007/s12298-023-01326-4.
ABSTRACT
The cytochrome b6f (cyt b6f) acts as a common linker of electron transport between photosystems I and II in oxygenic photosynthesis. PetM, one of eight subunits of the cyt b6f complex, is a small hydrophobic subunit at the outside periphery, the functional mechanism of which remains to be elucidated in higher plants. In this work, we found that unlike the PetM mutant in Synechocystis sp. PCC 6803, the Arabidopsis thaliana PetM mutant showed a bleached phenotype with yellowish leaves, block of photosynthetic electron transport and loss of photo-autotrophy, similar to the Arabidopsis PetC mutant. Although PetM is relatively conserved between higher plants and cyanobacteria, Synechocystis PetM could not rescue the PetM-knockout phenotype in Arabidopsis. We provide evidence that the Synechocystis PetM did not stably bind to the Arabidopsis cyt b6f complex. Based on these results, we suggest that PetM is required by Arabidopsis to maintain the function of the cyt b6f complex, likely through its close link with core subunits to form a tight 'fence' that stabilizes the core of the complex.
Subject(s)
Arabidopsis Proteins/genetics , Arabidopsis/physiology , Cytochrome b6f Complex/genetics , Mutation , Photosynthesis , Plant Leaves/genetics , Amino Acid Sequence , Arabidopsis/genetics , Arabidopsis Proteins/chemistry , Arabidopsis Proteins/metabolism , Color , Cytochrome b6f Complex/chemistry , Cytochrome b6f Complex/metabolism , Electron Transport , Phenotype , Sequence AlignmentABSTRACT
Salicylic acid (SA) plays pivotal role in plant defense against biotrophic and hemibiotrophic pathogens. Tremendous progress has been made in the field of SA biosynthesis and SA signaling pathways over the past three decades. Among the key immune players in SA signaling pathway, NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) functions as a master regulator of SA-mediated plant defense. The function of NPR1 as an SA receptor has been controversial; however, after years of arguments among several laboratories, NPR1 has finally been proven as one of the SA receptors. The function of NPR1 is strictly regulated via post-translational modifications and transcriptional regulation that were recently found. More recent advances in NPR1 biology, including novel functions of NPR1 and the structure of SA receptor proteins, have brought this field forward immensely. Therefore, based on these recent discoveries, this review acts to provide a full picture of how NPR1 functions in plant immunity and how NPR1 gene and NPR1 protein are regulated at multiple levels. Finally, we also discuss potential challenges in future studies of SA signaling pathway.
Subject(s)
Plant Immunity/physiology , Plant Proteins/immunology , Plant Proteins/metabolism , Salicylic Acid/metabolism , Arabidopsis Proteins/immunology , Gene Expression Regulation, Plant , Phosphorylation , Plant Proteins/chemistry , Plant Proteins/genetics , Salicylic Acid/immunology , Sumoylation , UbiquitinationABSTRACT
Fusarium graminearum is a destructive fungal pathogen that threatens the production and quality of wheat, and controlling this pathogen is a significant challenge. As the cost-effective homolog of melatonin, 5-methoxyindole showed strong activity against F. graminearum. In the present study, our results showed the strong adverse activity of 5-methoxyindole against F. graminearum by inhibiting its growth, formation, and conidia germination. In addition, 5-methoxyindole could induce malformation, reactive oxygen species (ROS) accumulation, and cell death in F. graminearum hyphae and conidia. In response to 5-methoxyindole, F. graminearum genes involved in scavenging reactive oxygen species were significantly downregulated. Overall, these findings reveal the mechanism of antifungal action of melatonin-homolog 5-methoxyindole. To the best of our knowledge, this is the first report that a novel melatonin homolog confers strong antifungal activity against F. graminearum, and 5-methoxyindole is a potential compound for protecting wheat plants from F. graminearum infection.
Subject(s)
Fusarium/drug effects , Indoles/pharmacology , Down-Regulation/drug effects , Fungal Proteins/genetics , Fusarium/growth & development , Fusarium/metabolism , Melatonin/chemistry , Melatonin/pharmacology , Microbial Sensitivity Tests , Reactive Oxygen Species/metabolismABSTRACT
In chloroplasts, insertion of proteins with multiple transmembrane domains (TMDs) into thylakoid membranes usually occurs in a co-translational manner. Here, we have characterized a thylakoid protein designated FPB1 (Facilitator of PsbB biogenesis1) which together with a previously reported factor PAM68 (Photosynthesis Affected Mutant68) is involved in assisting the biogenesis of CP47, a subunit of the Photosystem II (PSII) core. Analysis by ribosome profiling reveals increased ribosome stalling when the last TMD segment of CP47 emerges from the ribosomal tunnel in fpb1 and pam68. FPB1 interacts with PAM68 and both proteins coimmunoprecipitate with SecY/E and Alb3 as well as with some ribosomal components. Thus, our data indicate that, in coordination with the SecY/E translocon and the Alb3 integrase, FPB1 synergistically cooperates with PAM68 to facilitate the co-translational integration of the last two CP47 TMDs and the large loop between them into thylakoids and the PSII core complex.
Subject(s)
Photosystem II Protein Complex , Thylakoids , Chloroplasts/metabolism , Photosystem II Protein Complex/genetics , Photosystem II Protein Complex/metabolism , Ribosomes/metabolism , Thylakoids/metabolismABSTRACT
Frailty, a multidimensional indicator of suboptimal aging, reflects cumulative declines across multiple physiological systems. Although age-related changes have been reported in gut microbiota, their role in healthy aging remains unclear. In this study, we calculated frailty index (FI) from 33 health-related items to reflect the overall health status of 1,821 older adults (62-96 years, 55% female) and conducted multi-omics analysis using gut metagenomic sequencing data and plasma metabolomic data. We identified 18 microbial species and 17 metabolites shifted along with frailty severity, with stronger links observed in females. The associations of nine species, including various Clostridium species and Faecalibacterium prausnitzii, with FI were reproducible in two external populations. Plasma glycerol levels, white blood cell count and kidney function partially mediated these associations. A composite microbial score derived from FI significantly predicted 2-year mortality (adjusted hazard ratio across extreme quartiles, 2.86; 95% confidence interval, 1.38-5.93), highlighting the potential of microbiota-based strategies for risk stratification in older adults.
ABSTRACT
The low-carbohydrate ketogenic diet (KD) has long been practiced for weight loss, but the underlying mechanisms remain elusive. Gut microbiota and metabolites have been suggested to mediate the metabolic changes caused by KD consumption, although the particular gut microbes or metabolites involved are unclear. Here, we show that KD consumption enhances serum levels of taurodeoxycholic acid (TDCA) and tauroursodeoxycholic acid (TUDCA) in mice to decrease body weight and fasting glucose levels. Mechanistically, KD feeding decreases the abundance of a bile salt hydrolase (BSH)-coding gut bacterium, Lactobacillus murinus ASF361. The reduction of L. murinus ASF361 or inhibition of BSH activity increases the circulating levels of TDCA and TUDCA, thereby reducing energy absorption by inhibiting intestinal carbonic anhydrase 1 expression, which leads to weight loss. TDCA and TUDCA treatments have been found to protect against obesity and its complications in multiple mouse models. Additionally, the associations among the abovementioned bile acids, microbial BSH and metabolic traits were consistently observed both in an observational study of healthy human participants (n = 416) and in a low-carbohydrate KD interventional study of participants who were either overweight or with obesity (n = 25). In summary, we uncover a unique host-gut microbiota metabolic interaction mechanism for KD consumption to decrease body weight and fasting glucose levels. Our findings support TDCA and TUDCA as two promising drug candidates for obesity and its complications in addition to a KD.
Subject(s)
Bile Acids and Salts , Diet, Ketogenic , Gastrointestinal Microbiome , Obesity , Animals , Obesity/metabolism , Obesity/prevention & control , Obesity/etiology , Mice , Bile Acids and Salts/metabolism , Humans , Gastrointestinal Microbiome/drug effects , Taurochenodeoxycholic Acid/pharmacology , Male , Energy Intake , Mice, Inbred C57BL , Taurodeoxycholic Acid/metabolismABSTRACT
Benzene is an established leukotoxin and leukemogen in humans. We have previously reported that exposure of workers to benzene and to benzene metabolite hydroquinone in cultured cells induced DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to mediate the cellular response to DNA double strand break (DSB) caused by DNA-damaging metabolites. In this study, we used a new, small molecule, a selective inhibitor of DNA-PKcs, 2-(morpholin-4-yl)-benzo[h]chomen-4-one (NU7026), as a probe to analyze the molecular events and pathways in hydroquinone-induced DNA DSB repair and apoptosis. Inhibition of DNA-PKcs by NU7026 markedly potentiated the apoptotic and growth inhibitory effects of hydroquinone in proerythroid leukemic K562 cells in a dose-dependent manner. Treatment with NU7026 did not alter the production of reactive oxygen species and oxidative stress by hydroquinone but repressed the protein level of DNA-PKcs and blocked the induction of the kinase mRNA and protein expression by hydroquinone. Moreover, hydroquinone increased the phosphorylation of Akt to activate Akt, whereas co-treatment with NU7026 prevented the activation of Akt by hydroquinone. Lastly, hydroquinone and NU7026 exhibited synergistic effects on promoting apoptosis by increasing the protein levels of pro-apoptotic proteins Bax and caspase-3 but decreasing the protein expression of anti-apoptotic protein Bcl-2. Taken together, the findings reveal a central role of DNA-PKcs in hydroquinone-induced hematotoxicity in which it coordinates DNA DSB repair, cell cycle progression, and apoptosis to regulate the response to hydroquinone-induced DNA damage.
Subject(s)
Apoptosis/physiology , Benzene/toxicity , Chromones/pharmacology , DNA Damage/drug effects , DNA Repair/physiology , DNA-Activated Protein Kinase/metabolism , Morpholines/pharmacology , Apoptosis/drug effects , Catalysis , DNA Damage/genetics , DNA Repair/drug effects , DNA-Activated Protein Kinase/antagonists & inhibitors , Humans , K562 Cells , Protein SubunitsABSTRACT
Plants have multiple mechanisms to maintain efficient photosynthesis. Photosynthetic cyclic electron transports around photosystem I (CET), which includes the PGR5/PGRL1 and NDH pathways, and photorespiration play a crucial role in photosynthetic efficiency. However, how these two mechanisms are functionally linked is not clear. In this study, we revealed that photorespiration could compensate for the function of CET in efficient photosynthesis by comparison of the growth phenotypes, photosynthetic properties monitored with chlorophyll fluorescence parameters and photosynthetic oxygen evolution in leaves and photorespiratory activity monitored with the difference of photosynthetic oxygen evolution rate under high and low concentration of oxygen conditions between the deleted mutant PGR5 or PGRL1 under NDH defective background (pgr5 crr2 or pgrl1a1b crr2). Both CET mutants pgr5 crr2 and pgrl1a1b crr2 displayed similar suppression effects on photosynthetic capacities of light reaction and growth phenotypes under low light conditions. However, the total CET activity and photosynthetic oxygen evolution of pgr5 crr2 were evidently lower than those of pgrl1a1b crr2, accompanied by the upregulation of photorespiratory activity under low light conditions, resulting in severe suppression of photosynthetic capacities of light reaction and finally photodamaged phenotype under high light or fluctuating light conditions. Based on these findings, we suggest that photorespiration compensates for the loss of CET functions in the regulation of photosynthesis and that coordination of both mechanisms is essential for maintaining the efficient operation of photosynthesis, especially under stressed conditions.
ABSTRACT
Based on published information, the occurrence and development of Alzheimer's disease (AD) are potentially related to gut microbiota changes. Donepezil hydrochloride (DH), which enhances cholinergic activity by blocking acetylcholinesterase (AChE), is one of the first-line drugs for AD treatment approved by the Food and Drug Administration (FDA) of the USA. However, the potential link between the effects of DH on the pathophysiological processes of AD and the gut microbiota remains unclear. In this study, pathological changes in the brain and colon, the activities of superoxide dismutase (SOD) and AChE, and changes in intestinal flora were observed. The results showed that Aß deposition in the prefrontal cortex and hippocampus of AD mice was significantly decreased, while colonic inflammation was significantly alleviated by DH treatment. Concomitantly, SOD activity was significantly improved, while AChE was significantly reduced after DH administration. In addition, the gut microbiota community composition of AD mice was significantly altered after DH treatment. The relative abundance of Akkermansia in the AD group was 54.8% higher than that in the N group. The relative abundance of Akkermansia was increased by 18.3% and 53.8% in the AD_G group and the N_G group, respectively. Interestingly, Akkermansia showed a potential predictive value and might be a biomarker for AD. Molecular docking revealed the binding mode and major forces between DH and membrane proteins of Akkermansia. The overall results suggest a novel therapeutic mechanism for treating AD and highlight the critical role of gut microbiota in AD pathology.
ABSTRACT
A tuning fork gyroscope (TFG) with orthogonal thin-walled round holes in the driving and sensing directions is proposed to improve sensitivity. The thin walls formed by through holes produce stress concentration, transforming the small displacement of tuning fork vibration into a large concentrated strain. When piezoelectric excitation or detection is carried out here, the driving vibration displacement and detection output voltage can be increased, thereby improving sensitivity. Besides, quadrature coupling can be suppressed because the orthogonal holes make the optimal excitation and detection positions in different planes. The finite element method is used to verify the benefits of the holes, and the parameters are optimized for better performance. The experimental results show that the sensitivity of the prototype gyroscope with a driving frequency of 890.68 Hz is 100.32 mV/(°/s) under open-loop driving and detection, and the rotation rate can be resolved at least 0.016 (°/s)/Hz, which is about 6.7 times better than that of the conventional TFG. In addition, the quadrature error is reduced by 2.7 times. The gyroscope has a simple structure, high reliability, and effectively improves sensitivity, which is helpful to guide the optimization of piezoelectric gyroscopes and derived MEMS gyroscopes.
ABSTRACT
Background: Alterations in the gut microbiota have been observed in patients with pulmonary hypertension (PH), though whether the roles of the gut microbiota in PH at different altitudes are the same is unknown. This study aims to evaluate the associations of the gut microbiome with PH in highlanders and lowlanders. Methods: PH patients and controls were recruited from those who permanently live on the Tibetan plateau (highlanders) or the plains (lowlanders), and underwent transthoracic echocardiography close to their altitude of residence (at 5070â m for highlanders versus6â m for lowlanders). The gut microbiome was profiled using metagenomic shotgun sequencing. Results: In total, 13 PH patients (46% highlanders) and 88 controls (70% highlanders) were included. The overall microbial composition was different in PH patients compared to controls (p=0.003). Notably, among lowlanders, a composite microbial score of pro-atherosclerotic trimethylamine-producing species was increased in PH patients compared with that in controls (p=0.028), while among highlanders no such difference was observed (p=0.087). Another composite gut microbial score including eight species of Lactobacillus, which has shown beneficial effects on cardiovascular functions, was higher in highlanders than lowlanders (p<0.01). Furthermore, this score tended to be lower in PH patients than controls among highlanders (p=0.056) but not among lowlanders (p=0.840). In addition, the gut microbiome showed a good performance in distinguishing PH patients from controls in both lowlanders and highlanders. Conclusions: Our study reported differently altered gut microbiome profiles between highland and lowland PH patients, highlighting the distinct microbial mechanism in PH in highlanders compared with lowlanders.
ABSTRACT
Though gut microbiome disturbance may be involved in the etiology of gestational diabetes mellitus (GDM), data on the gut microbiome's dynamic change during pregnancy and associations with gestational glucose metabolism are still inadequate. In this prospective study comprising 120 pairs of GDM patients and matched pregnant controls, a decrease in the diversity of gut microbial species and changes in the microbial community composition with advancing gestation are found in controls, while no such trends are observed in GDM patients. Multivariable analysis identifies 10 GDM-related species (e.g., Alistipes putredinis), and the integrated associations of these species with glycemic traits are modified by habitual intake of fiber-rich plant foods. In addition, the microbial metabolic potentials related to fiber fermentation (e.g., mannan degradation pathways) and their key enzymes consistently emerge as associated with both GDM status and glycemic traits. Microbial features especially those involved in fiber fermentation, provide an incremental predictive value in a prediction model with established risk factors of GDM. These data suggest that the gut microbiome remodeling with advancing gestation is different in GDM patients compared with controls, and dietary fiber fermentation contributes to the influence of gut microbiome on gestational glycemic regulation.
Subject(s)
Diabetes, Gestational , Gastrointestinal Microbiome , Pregnancy , Female , Humans , Prospective Studies , Case-Control Studies , GlucoseABSTRACT
In land-plant chloroplasts, the grana play multiple roles in photosynthesis, including the potential increase of photosynthetic capacity in light and enhancement of photochemical efficiency in shade. However, the molecular mechanisms of grana formation remain elusive. Here, we report a novel gene, Grana-Deficient Chloroplast1 (GDC1), required for chloroplast grana formation in Arabidopsis (Arabidopsis thaliana). In the chloroplast of knockout mutant gdc1-3, only stromal thylakoids were observed, and they could not stack together to form appressed grana. The mutant exhibited seedling lethality with pale green cotyledons and true leaves. Further blue native-polyacrylamide gel electrophoresis analysis indicated that the trimeric forms of Light-Harvesting Complex II (LHCII) were scarcely detected in gdc1-3, confirming previous reports that the LHCII trimer is essential for grana formation. The Lhcb1 protein, the major component of the LHCIIb trimer, was substantially reduced, and another LHCIIb trimer component, Lhcb2, was slightly reduced in the gdc1-3 mutant, although their transcription levels were not altered in the mutant. This suggests that defective LHCII trimer formation in gdc1-3 is due to low amounts of Lhcb1 and Lhcb2. GDC1 encodes a chloroplast protein with an ankyrin domain within the carboxyl terminus. It was highly expressed in Arabidopsis green tissues, and its expression was induced by photosignaling pathways. Immunoblot analysis of the GDC1-green fluorescent protein (GFP) fusion protein in 35S::GDC1-GFP transgenic plants with GFP antibody indicates that GDC1 is associated with an approximately 440-kD thylakoid protein complex instead of the LHCII trimer. This shows that GDC1 may play an indirect role in LHCII trimerization during grana formation.
Subject(s)
Arabidopsis Proteins/chemistry , Arabidopsis Proteins/genetics , Arabidopsis/genetics , Arabidopsis/metabolism , Genes, Plant/genetics , Thylakoids/metabolism , Amino Acid Sequence , Ankyrins , Arabidopsis/ultrastructure , Arabidopsis Proteins/metabolism , Chlorophyll/metabolism , Cloning, Molecular , Gene Expression Regulation, Plant , Light-Harvesting Protein Complexes/chemistry , Light-Harvesting Protein Complexes/metabolism , Molecular Sequence Data , Mutation/genetics , Phylogeny , Plant Leaves/metabolism , Plant Leaves/ultrastructure , Protein Multimerization , Protein Structure, Tertiary , Protein Transport , Thylakoids/genetics , Thylakoids/ultrastructureABSTRACT
The high-frequency eddy current loss limits the output speed of the giant magnetostrictive actuator (GMA). This paper investigates a GMA using a laminated silicon steel core. Compared with the integral silicon steel core, the laminated silicon steel core can reduce the equivalent conductivity and eddy currents. The laminated structure reduces the magnetic reluctance of the core and increases the magnetic field intensity in the giant magnetostrictive material rod. Therefore, the actuator can output large vibration amplitude under high-frequency magnetic field. At the sinusoidal excitation current of 35 A (rms) @ 2 kHz, the output vibration amplitude of the actuator using the laminated silicon steel core is 11.1 µm @ 4 kHz, which is 44.2% higher than that of the actuator with the integral silicon steel core. This indicates that the laminated structure of the magnetic core is beneficial to improve the output speed of GMA.
ABSTRACT
Chloroplast development involves the coordinated expression of both plastids- and nuclear-encoded genes in higher plants. However, the underlying mechanism still remains largely unknown. In this study, we isolated and characterized an Arabidopsis mutant with an albino lethality phenotype named RNA processing 8 (rp8). Genetic complementation analysis demonstrated that the gene AT4G37920 (RP8) was responsible for the mutated phenotype. The RP8 gene was strongly expressed in photosynthetic tissues at both transcription and translation protein levels. The RP8 protein is localized in the chloroplast and associated with the thylakoid. Disruption of the RP8 gene led to a defect in the accumulation of the rpoA mature transcript, which reduced the level of the RpoA protein, and affected the transcription of PEP-dependent genes. The abundance of the chloroplast rRNA, including 23S, 16S, 4.5S, and 5S rRNA, were reduced in the rp8 mutant, respectively, and the amounts of chloroplast ribosome proteins, such as, PRPS1(uS1c), PRPS5(uS5c), PRPL2 (uL2c), and PRPL4 (uL4c), were substantially decreased in the rp8 mutant, which indicated that knockout of RP8 seriously affected chloroplast translational machinery. Accordingly, the accumulation of photosynthetic proteins was seriously reduced. Taken together, these results indicate that the RP8 protein plays an important regulatory role in the rpoA transcript processing, which is required for the expression of chloroplast genes and chloroplast development in Arabidopsis.
ABSTRACT
Natural ß-carboline alkaloids are ideal models for the discovery of pharmaceutically important entities. Various 1-substituted ß-carbolines were synthesized from commercially inexpensive tryptophan and demonstrated significant in vitro antifungal activity against G. graminis. Significantly, compound 4m (EC50 = 0.45 µM) with carboxamide at 1-position displayed the best efficacy and nearly 20 folds enhancement in antifungal potential compared to Silthiopham (EC50 = 8.95 µM). Moreover, compounds 6, 7, and 4i exhibited excellent in vitro antifungal activities and in vivo protective and curative activities against B. cinerea and F. graminearum. Preliminary mechanism studies revealed that compound 4m caused reactive oxygen species accumulation, cell membrane destruction, and deregulation of histone acetylation. These findings indicated that 1-carbamoyl ß-carboline can be selected as a promising model for the discovery of novel and broad-spectrum fungicide candidates.