The RPT2a-MET1 axis regulates TERMINAL FLOWER1 to control inflorescence meristem indeterminacy in Arabidopsis.

Plant inflorescence architecture is determined by inflorescence meristem (IM) activity and controlled by genetic mechanisms associated with environmental factors. In Arabidopsis (Arabidopsis thaliana), TERMINAL FLOWER1 (TFL1) is expressed in the IM and is required to maintain indeterminate growth, whereas LEAFY (LFY) is expressed in the floral meristems (FMs) formed at the periphery of the IM and is required to activate determinate floral development. Here, we address how Arabidopsis indeterminate inflorescence growth is determined. We show that the 26S proteasome subunit REGULATORY PARTICLE AAA-ATPASE 2a (RPT2a) is required to maintain the indeterminate inflorescence architecture in Arabidopsis. rpt2a mutants display reduced TFL1 expression levels and ectopic LFY expression in the IM and develop a determinate zigzag-shaped inflorescence. We further found that RPT2a promotes DNA METHYLTRANSFERASE1 degradation, leading to DNA hypomethylation upstream of TFL1 and high TFL1 expression levels in the wild-type IM. Overall, our work reveals that proteolytic input into the epigenetic regulation of TFL1 expression directs inflorescence architecture in Arabidopsis, adding an additional layer to stem cell regulation.

Direct White-Light Emitting From a Single Metal-Organic Framework with Dual Phosphorescence Peaks.

Single component white-light-emitting (SCWLE) materials are extremely desired in the field of solid-state lighting. However, pure-phosphorescent SCWLE has rarely been reported. Herein, one halogen-bonding-containing MOF [Cd(5-BIPA)(phen)] (1) has been synthesized, which shows efficient white-light emission originating from dual phosphorescence bands with different wavelengths and lifetimes. The fabrication of a phosphor-converted white-light-emitting diode device driven by pulsing current enables this MOF to be a promising phosphor.

Fast photocatalytic degradation of rhodamine B using indium-porphyrin based cationic MOF under visible light irradiation.

A broad light-harvesting range and efficient charge separation are two main ways to enhance the visible photocatalytic performance of semiconductors. Herein, an ionic porphyrin MOF [In(TPyP)]·(NO3) (1) (TPyP = 5,10,15,20-tetrakis(4-pyridyl)-21H,23H-porphyrin) was synthesized via in situ metalation. The orderly arranged porphyrin photosensitizer and the internal electric field between the MOF host and NO3- guests enable effective visible light response and electron-hole separation. Consequently, the as-synthesized MOF shows efficient photocatalytic degradation of rhodamine B (RhB), methyl orange (MO) and methylene blue (MB) organic pollutants. It can degrade 99.07% of RhB within only 20 minutes under visible light irradiation (λ > 420 nm) with a high chemical reaction rate constant of 0.2400 min-1. The photocatalytic activity of the title MOF is more efficient than those of other reported MOFs, COFs and even inorganic semiconductors. The reusability, energy level, band gap, charge distribution and main degradation mechanisms of the photocatalyst were well studied.

Hypertrophied myocardium is vulnerable to ischemia/reperfusion injury and refractory to rapamycin-induced protection due to increased oxidative/nitrative stress.

Left ventricular hypertrophy (LVH) is causally related to increased morbidity and mortality following acute myocardial infarction (AMI) via still unknown mechanisms. Although rapamycin exerts cardioprotective effects against myocardial ischemia/reperfusion (MI/R) injury in normal animals, whether rapamycin-elicited cardioprotection is altered in the presence of LVH has yet to be determined. Pressure overload induced cardiac hypertrophied mice and sham-operated controls were exposed to AMI by coronary artery ligation, and treated with vehicle or rapamycin 10 min before reperfusion. Rapamycin produced marked cardioprotection in normal control mice, whereas pressure overload induced cardiac hypertrophied mice manifested enhanced myocardial injury, and was refractory to rapamycin-elicited cardioprotection evidenced by augmented infarct size, aggravated cardiomyocyte apoptosis, and worsening cardiac function. Rapamycin alleviated MI/R injury via ERK-dependent antioxidative pathways in normal mice, whereas cardiac hypertrophied mice manifested markedly exacerbated oxidative/nitrative stress after MI/R evidenced by the increased iNOS/gp91phox expression, superoxide production, total NO metabolites, and nitrotyrosine content. Moreover, scavenging superoxide or peroxynitrite by selective gp91phox assembly inhibitor gp91ds-tat or ONOO- scavenger EUK134 markedly ameliorated MI/R injury, as shown by reduced myocardial oxidative/nitrative stress, alleviated myocardial infarction, hindered cardiomyocyte apoptosis, and improved cardiac function in aortic-banded mice. However, no additional cardioprotective effects were achieved when we combined rapamycin and gp91ds-tat or EUK134 in ischemic/reperfused hearts with or without LVH. These results suggest that cardiac hypertrophy attenuated rapamycin-induced cardioprotection by increasing oxidative/nitrative stress and scavenging superoxide/peroxynitrite protects the hypertrophied heart from MI/R.

Aliskiren ameliorates pressure overload-induced heart hypertrophy and fibrosis in mice.

AIM: Aliskiren (ALK) is a renin inhibitor that has been used in the treatment of hypertension. The aim of this study was to determine whether ALK could ameliorate pressure overload-induced heart hypertrophy and fibrosis, and to elucidate the mechanisms of action. METHODS: Transverse aortic constriction (TAC) was performed in mice to induce heart pressure overload. ALK (150 mg·kg(-1)·d(-1), po), the autophagy inhibitor 3-methyladenine (10 mg·kg(-1) per week, ip) or the PKCßI inhibitor LY333531 (1 mg·kg(-1)·d-(1), po) was administered to the mice for 4 weeks. Heart hypertrophy, fibrosis and function were evaluated based on echocardiography, histological and biochemical measurements. Mechanically stretched cardiomyocytes of rats were used for in vitro experiments. The levels of signaling proteins were measured using Western blotting, while the expression of the relevant genes was analyzed using real-time QRT-PCR. RESULTS: TAC induced marked heart hypertrophy and fibrosis, accompanied by high levels of Ang II in plasma and heart, and by PKCßI/α and ERK1/2 phosphorylation in heart. Meanwhile, TAC induced autophagic responses in heart, i.e. increases in autophagic structures, expression of Atg5 and Atg16 L1 mRNAs and LC3-II and Beclin-1 proteins. These pathological alterations in TAC-mice were significantly ameliorated or blocked by ALK administration. In TAC-mice, 3-methyladenine administration also ameliorated heart hypertrophy, fibrosis and dysfunction, while LY333531 administration inhibited ERK phosphorylation and autophagy in heart. In mechanically stretched cardiomyocytes, CGP53353 (a PKCßI inhibitor) prevented ERK phosphorylation and autophagic responses, while U0126 (an ERK inhibitor) blocked autophagic responses. CONCLUSION: ALK ameliorates heart hypertrophy, fibrosis and dysfunction in the mouse model in setting of chronic pressure overload, via suppressing Ang II-PKCßI-ERK1/2-regulated autophagy.

U-type π-conjugated phosphorescent ligand sensitized lanthanide metal-organic frameworks for efficient white-light-emitting diodes.

Lanthanide metal-organic framework (Ln-MOF) based phosphors for light-emitting diodes (LEDs) play an important role in the fields of solid-state lighting and display. The rational design of organic antennae to address the drawback of low extinction coefficients of the lanthanide ions is highly desired. In this work, we provide a new design strategy to achieve an energy transfer molecule with a through-space conjugated folded structure, which can strengthen the skeleton rigidity and facilitate triplet state energy transfer. Consequently, one U-type π-conjugated molecule 2,6-bis(3,5-dicarboxylphenoxy) pyridine (H4L) was selected as a light gatherer to sensitize lanthanide ions for the construction of Ln-MOFs [Ln(HL)(H2O)3]n (Eu-MOF and Tb-MOF), which exhibit a long-lived luminescence lifetime (0.88 ms for Eu-MOF and 1.31 ms for Tb-MOF) and high quantum yields (50.87% for Eu-MOF and 85.64% for Tb-MOF). Furthermore, a white LED device with a colour rendering index (89) was fabricated using the mixture of Ln-MOFs with a commercial blue phosphor.

Options for Engineering Apomixis in Plants.

In plants, embryogenesis and reproduction are not strictly dependent on fertilization. Several species can produce embryos in seeds asexually, a process known as apomixis. Apomixis is defined as clonal asexual reproduction through seeds, whereby the progeny is identical to the maternal genotype, and provides valuable opportunities for developing superior cultivars, as its induction in agricultural crops can facilitate the development and maintenance of elite hybrid genotypes. In this review, we summarize the current understanding of apomixis and highlight the successful introduction of apomixis methods into sexual crops. In addition, we discuss several genes whose overexpression can induce somatic embryogenesis as candidate genes to induce parthenogenesis, a unique reproductive method of gametophytic apomixis. We also summarize three schemes to achieve engineered apomixis, which will offer more opportunities for the realization of apomictic reproduction.

Hypertrophic preconditioning cardioprotection after myocardial ischaemia/reperfusion injury involves ALDH2-dependent metabolism modulation.

Brief episodes of ischaemia and reperfusion render the heart resistant to subsequent prolonged ischaemic insult, termed ischaemic preconditioning. Here, we hypothesized that transient non-ischaemic stress by hypertrophic stimulation would induce endogenous cardioprotective signalling and enhance cardiac resistance to subsequent ischaemic damage. Transient transverse aortic constriction (TAC) or Ang-Ⅱ treatment was performed for 3-7 days in male mice and then withdrawn for several days by either aortic debanding or discontinuing Ang-Ⅱ treatment, followed by subsequent exposure to regional myocardial ischaemia by in situ coronary artery ligation. Following ischaemia/reperfusion (I/R) injury, myocardial infarct size and apoptosis were markedly reduced and contractile function was significantly improved in the TAC preconditioning group compared with that in the control group. Similar results were observed in mice receiving Ang-Ⅱ infusion. Mechanistically, TAC preconditioning enhanced ALDH2 activity, promoted AMPK activation and improved mitochondrial energy metabolism by increasing myocardial OXPHOS complex expression, elevating the mitochondrial ATP content and improving viable myocardium glucose uptake. Moreover, TAC preconditioning significantly mitigated I/R-induced myocardial iNOS/gp91phox activation, inhibited endoplasmic reticulum stress and ameliorated mitochondrial impairment. Using a pharmacological approach to inhibit AMPK signalling in the presence or absence of preconditioning, we demonstrated AMPK-dependent protective mechanisms of TAC preconditioning against I/R injury. Furthermore, treatment with adenovirus-encoded ALDH2 partially emulated the actions of hypertrophic preconditioning, as evidenced by improved mitochondrial metabolism, inhibited oxidative stress-induced mitochondrial damage and attenuated cell death through an AMPK-dependent mechanism, whereas genetic ablation of ALDH2 abrogated the aforementioned actions of TAC preconditioning. The present study demonstrates that preconditioning with hypertrophic stress protects the heart from I/R injury via mechanisms that improve mitochondrial metabolism, reduce oxidative/nitrative stress and inhibit apoptosis. ALDH2 is obligatorily required for the development of cardiac hypertrophic preconditioning and acts as the mediator of this process.

Structural characterisation and antioxidant activity evaluation of phenolic compounds from cold-pressed Perilla frutescens var. arguta seed flour.

A total of 11 phenolic compounds, as well as sucrose (12) and tryptophan (13), were isolated from cold-pressed Perilla frutescens var. arguta seed flour using column chromatography, and their chemical structures were identified as 3'-dehydroxyl-rosmarinic acid-3-o-glucoside (1), rosmarinic acid-3-o-glucoside (2), rosmarinic acid (3), rosmarinic acid methyl ester (4), luteolin (5), luteolin-5-o-glucoside (6), apigenin (7), caffeic acid (8), caffeic acid-3-o-glucoside (9), vanillic acid (10) and cimidahurinine (11) using NMR and time-of-flight mass spectrometry. Of these components, compound 1 is novel, and this is the first report of compounds 10 and 11 in perilla seeds. HPLC quantification combined with antioxidant activity evaluation revealed that rosmarinic acid and rosmarinic acid-3-o-glucoside were the dominant phenolic antioxidants with strong antioxidant activities.

Fine encapsulation of dual-particle electronic ink by incorporating block copolymer for electrophoretic display application.

The design of the oppositely charged ink particles based on titanium dioxide and carbon black for the monochrome electrophoretic display (EPD) was reported. The white ink particles with acidic surface and black ink particles with basic surface were synthesized and sterically stabilized by long alkyl chains, which were charged oppositely by mixing with basic surfactant (OLOA 1200) and acidic surfactant (Span 80), respectively. The electrophoretic mobility and the Zeta potential were -3.87×10(-10)m(2)V(-1)s(-1) and -25.1 mV for the white ink particles, 3.79×10(-10)m(2)V(-1)s(-1) and 24.6 mV for the black ink particles. In addition, the block copolymer, poly(lauryl methacrylate)-b-poly(2-(dimethylamino)ethyl methacrylate) (PLMA-b-PDMAEMA) synthesized by atom transfer radical polymerization (ATRP), was first incorporated in the modification of the pigments for the fine encapsulation. Then, a stable dual-particle electronic ink with contrast ratio of 120:1 was prepared and encapsulated with the gelatin (GE)/sodium carboxymethylcellulose (NaCMC)/sodium dodecyl sulfate (SDS) microcapsules by complex coacervation method. Finally, the matrix character display prototype driven at a low voltage exhibited excellent performance, the contrast ratio of which was 8:1 at 9 V DC.

Chinese medicine Tongxinluo modulates vascular endothelial function by inducing eNOS expression via the PI-3K/Akt/HIF-dependent signaling pathway.

AIM OF THE STUDY: To investigate the molecular mechanisms whereby the Chinese medicinal compound Tongxinluo improves vascular endothelial function through studying the induction of endothelial nitric oxide synthase (eNOS) and its upstream signaling pathway. MATERIALS AND METHODS: Hyperhomocysteinemia was induced in Wistar rats by a methionine-rich diet followed by Tongxinluo treatment. The aorta ring was isolated for measuring vascular dilation of aorta and eNOS expression. Human umbilical vein endothelial cells (HUVECs) were transfected with AP-1, NF-κB, HRE or eNOS reporter plasmid followed by Tongxinluo exposure. Expression of the reporter genes was measured by luciferase assay. The level of eNOS was studied by western blot and the nitric oxide content was measured using the nitrate reductase method. HUVECs were also transiently transfected with the dominant negative mutant of HIF-1, PI-3K or Akt to explore the role of HIF and PI-3K/Akt pathway in eNOS induction by Tongxinluo. RESULTS: Tongxinluo could significantly up-regulate the expression of eNOS in the aortic tissue and improve the endothelium-dependent vasodilation of the aorta ring. Additionally, Tongxinluo at various doses could significantly enhance the expression of HRE and eNOS reporter gene as well as up-regulate the protein level of eNOS. Meanwhile, Tongxinluo caused a dose-dependent increase in the NO content in the supernatant of HUVECs. Suppression of HIF-1 activation by DN-HIF or inhibition of PI-3K/Akt pathway by ΔP85 or DN-Akt both attenuated HRE reporter gene activation and eNOS induction by Tongxinluo. CONCLUSION: Tongxinluo, a compound Chinese traditional medicine, up-regulates the expression of eNOS via the PI-3K/Akt/HIF-dependent signaling pathway, thus improving the endothelium-dependent vasodilation.