A CRY-BIC negative-feedback circuitry regulating blue light sensitivity of Arabidopsis.

Cryptochromes are blue light receptors that regulate various light responses in plants. Arabidopsis cryptochrome 1 (CRY1) and cryptochrome 2 (CRY2) mediate blue light inhibition of hypocotyl elongation and long-day (LD) promotion of floral initiation. It has been reported recently that two negative regulators of Arabidopsis cryptochromes, Blue light Inhibitors of Cryptochromes 1 and 2 (BIC1 and BIC2), inhibit cryptochrome function by blocking blue light-dependent cryptochrome dimerization. However, it remained unclear how cryptochromes regulate the BIC gene activity. Here we show that cryptochromes mediate light activation of transcription of the BIC genes, by suppressing the activity of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), resulting in activation of the transcription activator ELONGATED HYPOCOTYL 5 (HY5) that is associated with chromatins of the BIC promoters. These results demonstrate a CRY-BIC negative-feedback circuitry that regulates the activity of each other. Surprisingly, phytochromes also mediate light activation of BIC transcription, suggesting a novel photoreceptor co-action mechanism to sustain blue light sensitivity of plants under the broad spectra of solar radiation in nature

Overexpression of Arabidopsis thaliana brassinosteroid-related acyltransferase 1 gene induces brassinosteroid-deficient phenotypes in creeping bentgrass

Brassinosteroids (BRs) are naturally occurring steroidal hormones that play diverse roles in various processes during plant growth and development. Thus, genetic manipulation of endogenous BR levels might offer a way of improving the agronomic traits of crops, including plant architecture and stress tolerance. In this study, we produced transgenic creeping bentgrass (Agrostis stolonifera L.) overexpressing a BR-inactivating enzyme, Arabidopsis thaliana BR-related acyltransferase 1 (AtBAT1), which is known to catalyze the conversion of BR intermediates to inactive acylated conjugates. After putative transgenic plants were selected using herbicide resistance assay, genomic integration of the AtBAT1 gene was confirmed by genomic PCR and Southern blot analysis, and transgene expression was validated by northern blot analysis. The transgenic creeping bentgrass plants exhibited BR-deficient phenotypes, including reduced plant height with shortened internodes (i.e., semi-dwarf), reduced leaf growth rates with short, wide, and thick architecture, high chlorophyll contents, decreased numbers of vascular bundles, and large lamina joint bending angles (i.e., erect leaves). Subsequent analyses showed that the transgenic plants had significantly reduced amounts of endogenous BR intermediates, including typhasterol, 6-deoxocastasterone, and castasterone. Moreover, the AtBAT1 transgenic plants displayed drought tolerance as well as delayed senescence. Therefore, the results of the present study demonstrate that overexpression of an Arabidopsis BR-inactivating enzyme can reduce the endogenous levels of BRs in creeping bentgrass resulting in BR-deficient phenotypes, indicating that the AtBAT1 gene from a dicot plant is also functional in the monocot crop.111Ysciescopu

Adaptive Fuzzy Dynamic Surface Sliding Mode Position Control for a Robot Manipulator with Friction and Deadzone

Precise tracking positioning performance in the presence of both the deadzone and friction of a robot manipulator actuator is difficult to achieve by traditional control methodology without proper nonlinear compensation schemes. In this paper, we present a dynamic surface sliding mode control scheme combined with an adaptive fuzzy system, state observer, and parameter estimator to estimate the uncertainty, friction, and deadzone nonlinearities of a robot manipulator system. We design a dynamic surface sliding mode basic controller by systematic recursive design steps that yields several adaptive laws for the compensation of nonlinear friction, deadzone, and other unknown nonlinear dynamics. The boundedness and convergence of this closed-loop system are guaranteed by the Lyapunov stability theorem. Experiments on the Scorbot robot manipulator demonstrate the validity and effectiveness of the proposed control scheme

Electrical current suppression in Pd-doped vanadium pentoxide nanowires caused by reduction in PdO due to hydrogen exposure

Pd nanoparticle-doped vanadium pentoxide nanowires (Pd-VONs) were synthesized. Electrical current suppression was observed when the Pd-VON was exposed to hydrogen gas, which cannot be explained by the work function changes mentioned in previous report such as Pd-doped carbon nanotubes and SnO 2 nanowires. Using the x-ray photoelectron spectroscopy, we found that the reduction in PdO due to hydrogen exposure plays an important role in the current suppression of the Pd-VON.open4

Barrier protection via Toll-like receptor 2 signaling in porcine intestinal epithelial cells damaged by deoxynivalnol

Additional file 2. IPEC-J2 cells pretreated with TLR2 ligand maintained the expression of MCP-1, GM-CSF and TLR2 against DON exposure. IPEC-J2 cells pretreated with or without TLR2 ligand for 24 h were exposed to DON. (A) The bar graph showed the mRNA levels of porcine mcp-1, gm-csf measured using real time-PCR at 1 and 6 h after DON exposure (n = 3). (B) The mRNA levels of porcine tlr2 were measured using real-time quantitative PCR analysis at 6 h. NT represents no treatment. Expression of each mRNA was presented relative to the expression of housekeeping gene, gapdh (n = 3). *P < 0.05; **P < 0.01; ***P < 0.001, determined by one-way ANOVA with Tukey’s posttest

Congenital Heart Disease (Atrioventricular Septal Defect) in the Mouse with Trisomy 16

Failure of fusion between the superior and inferior cushions has usually been assumed to be the main morphogenetic event in producing hearts with deficient atrioventricular septation (atrioventricular septal, or endocardial cushion defects). Morphological studies on human autopsy specimens, however, showed that another consistent finding is the marked disproportion between the dimensions of the inlet and outlet of the left ventricle, which, until now, has no known developmental basis. We have studied the early formation of the hearts with atrioventricular septal defects, using a mouse model with trisomy 16. Animals were studied between the 10th and 19th days of gestation by stereomicroscopic examination, scanning electronmlcroscopy and the in-vitro incorporation of thymidine. The first detectable morphological abnormality of the heart in the trisomic mouse was observed on the 11th day, being a persistence of an infolding at the inferior atrioventricular junction. This infolding was present in both trisomic and eusomic animals on the 10th day. This morphology could be explained by a differential growth of the myocardium at the inferior atrioventricular junction, which was found to be a distinct zone with low incorporation of thymidine. On the 11th day, the inferior atrioventricular cushion was bigger in the trisomic hearts. The abnormalities of the cushions observed on the 12th day or later were deemed to be consequences of these primary defects. Sectioning of the heart from the left lateral aspect convincingly showed morphological changes of the superior and inferior cushion or bridging leaflets in this animal model. Abnormal endocardial cushions and abnormality in the proliferation index of the myocardium at the inferior atrioventricular junction play more significant roles in the formation of the hearts with deficient atrioventricular septation, than the abnormalities found in the atrioventricular cushions