The grain yield regulator NOG1 plays a dual role in latitudinal adaptation and cold tolerance during rice domestication.

Rice originated in tropical and subtropical regions and is distributed worldwide. Low temperature is one of the most critical abiotic stresses affecting grain yield and geographical distribution of rice. It is vital to elucidate the molecular mechanism of chilling tolerance in rice for ensuring cereals production. Previously we isolated the domestication-related gene NOG1 which affects rice grain number and yield. In this study, we specified that rice varieties harboring high-yielding NOG1 allele are more distributed in low-latitude regions. Additionally, we observed NOG1 influences the chilling tolerance of rice. Through genome-wide transcriptional analysis after cold treatment at 10°C, there were 717 differentially expressed genes (DEGs) in nog1 near-isogenic lines compared with the control Guichao 2, including 432 up-regulated DEGs and 284 down-regulated DEGs. Gene ontology annotations and KEGG enrichment analysis of DEGs showed that various biological processes and signaling pathways were related to cold stress, such as lipid metabolism and genetic information processing. These results provide new insights into the mechanism of chilling tolerance in rice and the molecular basis of environmental adaptation during rice domestication.

Interactive Effects of Light Quality and Temperature on Arabidopsis Growth and Immunity.

We report here the interactive effects of three light qualities (white, red and blue) and three growth temperatures (16�C, 22�C and 28�C) on rosette growth, hypocotyl elongation and disease resistance in Arabidopsis thaliana. While an increase in temperature promotes hypocotyl elongation irrespective of light quality, the effects of temperature on rosette growth and disease resistance are dependent on light quality. Maximum rosette growth rate under white, red and blue light are observed at 28�C, 16�C and 22�C, respectively. The highest disease resistance is observed at 16�C under all three light conditions, but the highest susceptibility is observed at 28�C for white light and 22�C for red and blue light. Interestingly, rosette growth is inhibited by phytochrome B (PHYB) under blue light at 28�C and by cryptochromes (CRYs) under red light at 16�C. In addition, disease resistance is inhibited by PHYB under blue light and promoted by CRYs under red light. Therefore, this study reveals a complex interaction between light and temperature in modulating rosette growth and disease resistance as well as the contribution of PHYB and CRY to disease resistance.

Salvia Miltiorrhiza Bge.f.alba Ameliorates the Progression of Monocrotaline-Induced Pulmonary Hypertension by Protecting Endothelial Injury in Rats.

Pulmonary hypertension (PH) is a life-threatening disease that is characterized by elevated pulmonary blood pressure, abnormally thickened pulmonary arteries, and right ventricular hypertrophy. Monocrotaline (MCT) has been used to generate an experimental model of PH in rats, with PH initiated from injuries of lung vascular endothelium. Salvia Miltiorrhiza Bge.f.alba is a widely used traditional herb in China, known to exert protective effects on vascular endothelial cell injury in animal experiments. However, the role of Salvia Miltiorrhiza Bge.f.alba in PH remains unclear. Thus, we investigated the effects of the aqueous extract of Salvia Miltiorrhiza Bge.f.alba (AESM) on MCT-induced PH and explored the pertinent mechanism. PH was induced in rats by a single subcutaneous injection of MCT (60 mg/kg body weight). Low or high dose (4.6 g/kg or 14 g/kg body weight) of AESM was then administered orally for 21 days to PH rats. Hemodynamic study showed that AESM reduced mean pulmonary artery pressure and improved right ventricle function. Lung pathological analysis revealed that AESM reduced wall thickness and lumen stenosis of pulmonary vessels. Also AESM ameliorated right ventricular hypertrophy. Measurement of biochemical parameters indicated that AESM decreased endothelin-1 and thromboxane A2 in plasma and increased nitrogen monoxide and prostacyclin in the plasma and reduced the increase of transforming growth factor ß1 in lung tissue. Our results suggest that AESM may ameliorate the progression of MCT-induced PH in rats, at least in part by its protective effect on endothelial injury. Therefore, Salvia Miltiorrhiza Bge.f.alba could be useful in the treatment of PH.

Single-shot fabrication of waveguide ternary gratings with narrow-band optical response.

Single-shot fabrication of three sets of nano-scale grating structures with different periods is reported, which are constructed on a glass substrate coated with a waveguide layer made of 200-nm-thick indium tin oxide (ITO). Multiple waveguide resonance modes are observed in the visible spectral range with a bandwidth as narrow as 10 nm. Angle-resolved tuning properties of these resonance modes enable simultaneous three-color optical response of the nanodevice to cover the whole visible spectrum. This implies very simple methods for the potential design and realization of flexible optoelectronic devices.

InGaZnO semiconductor thin film fabricated using pulsed laser deposition.

The InGaZnO thin films are fabricated on the quartz glass using pulsed laser deposition (PLD), where the target is prepared by mixing the Ga(2)O(3), In(2)O(3), and ZnO powders at a mol ratio of 1:1:8 before the solid-state reactions in a tube furnace at the atmospheric pressure. The product thin films were characterized comprehensively by X-ray diffraction, atomic force microscopy, Hall-effect investigation, and X-ray photoelectron spectroscopy. Thus, we demonstrate semiconductor thin-film materials with high smoothness, high transmittance in visible region, and excellent electrical properties.

Mutation of a conserved asparagine in the I-like domain promotes constitutively active integrins alphaLbeta2 and alphaIIbbeta3.

The leukocyte beta2 integrins are heterodimeric adhesion receptors required for a functional immune system. Many leukocyte adhesion deficiency-1 (LAD-1) mutations disrupt the expression and function of beta2 integrins. Herein, we further characterized the LAD-1 mutation N329S in the beta2 inserted (I)-like domain. This mutation converted alphaLbeta2 from a resting into a high affinity conformer because alphaLbeta2N329S transfectants adhered avidly to ligand intercellular adhesion molecule (ICAM)-3 in the absence of additional activating agent. An extended open conformation is adopted by alphaLbeta2N329S because of its reactivity with the beta2 activation reporter monoclonal antibodies MEM148 and KIM127. A corresponding mutation in beta3 generated constitutively active alphaIIbbeta3 that adhered to fibrinogen. This Asn is conserved in all human beta subunits, and it resides before the last helix of the I-like domain, which is known to be important in activation signal propagation. By mutagenesis studies and review of existing integrin structures, we conjectured that this conserved Asn may have a primary role in shaping the I-like domain by stabilizing the conformation of the alpha7 helix and the beta6-alpha7 loop in the I-like domain.

Down-regulation of integrin alpha M beta 2 ligand-binding function by the urokinase-type plasminogen activator receptor.

The cell adhesion molecule integrin alphaMbeta2 associates with the urokinase-type plasminogen activator receptor (uPAR) on monocytes and neutrophils. uPAR also associates with members of the beta1 and beta3 integrins, and it modulates the ligand-binding function of these integrins. In this study, we showed that co-expressing uPAR with alphaMbeta2 in 293 transfectants down-regulated the ligand-binding capacity of alphaMbeta2 to denatured protein, fibrinogen, and intercellular adhesion molecule 1 (ICAM-1). Migration of transfectants on fibrinogen mediated by alphaMbeta2 was reduced in the presence of uPAR. In addition, the constitutive ligand-binding property of an alphaMbeta2 mutant was attenuated by its association with uPAR. Co-immunoprecipitation analyses using a panel of alphaMbeta2-specific mAbs suggest shielding of the ligand-recognition site of alphaMbeta2 by uPAR.