Academia Sinica

About: Academia Sinica is a facility organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Gene. The organization has 52086 authors who have published 65998 publications receiving 1728114 citations. The organization is also known as: Central Research Academy.

Arabidopsis Hsa32, a Novel Heat Shock Protein, Is Essential for Acquired Thermotolerance during Long Recovery after Acclimation

Abstract: Plants and animals share similar mechanisms in the heat shock (HS) response, such as synthesis of the conserved HS proteins (Hsps). However, because plants are confined to a growing environment, in general they require unique features to cope with heat stress. Here, we report on the analysis of the function of a novel Hsp, heat-stress-associated 32-kD protein (Hsa32), which is highly conserved in land plants but absent in most other organisms. The gene responds to HS at the transcriptional level in moss (Physcomitrella patens), Arabidopsis (Arabidopsis thaliana), and rice (Oryza sativa). Like other Hsps, Hsa32 protein accumulates greatly in Arabidopsis seedlings after HS treatment. Disruption of Hsa32 by T-DNA insertion does not affect growth and development under normal conditions. However, the acquired thermotolerance in the knockout line was compromised following a long recovery period (>24 h) after acclimation HS treatment, when a severe HS challenge killed the mutant but not the wild-type plants, but no significant difference was observed if they were challenged within a short recovery period. Quantitative hypocotyl elongation assay also revealed that thermotolerance decayed faster in the absence of Hsa32 after a long recovery. Similar results were obtained in Arabidopsis transgenic plants with Hsa32 expression suppressed by RNA interference. Microarray analysis of the knockout mutant indicates that only the expression of Hsa32 was significantly altered in HS response. Taken together, our results suggest that Hsa32 is required not for induction but rather maintenance of acquired thermotolerance, a feature that could be important to plants.

Genomic and Proteomic Analysis of Thirty-Nine Structural Proteins of Shrimp White Spot Syndrome Virus

Abstract: White spot syndrome virus (WSSV) virions were purified from the hemolymph of experimentally infected crayfish Procambarus clarkii, and their proteins were separated by 8 to 18% gradient sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to give a protein profile. The visible bands were then excised from the gel, and following trypsin digestion of the reduced and alkylated WSSV proteins in the bands, the peptide sequence of each fragment was determined by liquid chromatography-nano-electrospray ionization tandem mass spectrometry (LC-nanoESI-MS/MS) using a quadrupole/time-of-flight mass spectrometer. Comparison of the resulting peptide sequence data against the nonredundant database at the National Center for Biotechnology Information identified 33 WSSV structural genes, 20 of which are reported here for the first time. Since there were six other known WSSV structural proteins that could not be identified from the SDS-PAGE bands, there must therefore be a total of at least 39 (33 + 6) WSSV structural protein genes. Only 61.5% of the WSSV structural genes have a polyadenylation signal, and preliminary analysis by 3' rapid amplification of cDNA ends suggested that some structural protein genes produced mRNA without a poly(A) tail. Microarray analysis showed that gene expression started at 2, 6, 8, 12, 18, 24, and 36 hpi for 7, 1, 4, 12, 9, 5, and 1 of the genes, respectively. Based on similarities in their time course expression patterns, a clustering algorithm was used to group the WSSV structural genes into four clusters. Genes that putatively had common or similar roles in the viral infection cycle tended to appear in the same cluster.

Double parton scattering in [Formula presented] collisions at [Formula presented]

Abstract: A strong signal for double parton (DP) scattering is observed in a 16pb−1 sample of p¯p→γ/π0+3jets+X data from the CDF experiment at the Fermilab Tevatron. In DP events, two separate hard scatterings take place in a single p¯p collision. We isolate a large sample of data (∼14000events) of which 53% are found to be DP. The process-independent parameter of double parton scattering, σeff, is obtained without reference to theoretical calculations by comparing observed DP events to events with hard scatterings in separate p¯p collisions. The result σeff=(14.5±1.7−2.3+1.7)mb represents a significant improvement over previous measurements, and is used to constrain simple models of parton spatial density. The Feynman x dependence of σeff is investigated and none is apparent. Further, no evidence is found for kinematic correlations between the two scatterings in DP events.

Planck early results. XVIII. The power spectrum of cosmic infrared background anisotropies

Abstract: Using Planck maps of six regions of low Galactic dust emission with a total area of about 140 deg 2 , we determine the angular power spectra of cosmic infrared background (CIB) anisotropies from multipole � = 200 to � = 2000 at 217, 353, 545 and 857 GHz. We use 21-cm observations of Hi as a tracer of thermal dust emission to reduce the already low level of Galactic dust emission and use the 143 GHz Planck maps in these fields to clean out cosmic microwave background anisotropies. Both of these cleaning processes are necessary to avoid significant contamination of the CIB signal. We measure correlated CIB structure across frequencies. As expected, the correlation decreases with increasing frequency separation, because the contribution of high-redshift galaxies to CIB anisotropies increases with wavelengths. We find no significant difference between the frequency spectrum of the CIB anisotropies and the CIB mean, with ΔI/I = 15% from 217 to 857 GHz. In terms of clustering properties, the Planck data alone rule out the linear scale- and redshift-independent bias model. Non-linear corrections are significant. Consequently, we develop an alternative model that couples a dusty galaxy, parametric evolution model with a simple halo-model approach. It provides an excellent fit to the measured anisotropy angular power spectra and suggests that a different halo occupation distribution is required at each frequency, which is consistent with our expectation that each frequency is dominated by contributions from different redshifts. In our best-fit model, half of the anisotropy power at � = 2000 comes from redshifts z 2a t 353 and 217 GHz, respectively.

AMP-activated protein kinase functionally phosphorylates endothelial nitric oxide synthase Ser633.

Abstract: Endothelial nitric oxide synthase (eNOS) plays a central role in maintaining cardiovascular homeostasis by controlling NO bioavailability. The activity of eNOS in vascular endothelial cells (ECs) largely depends on posttranslational modifications, including phosphorylation. Because the activity of AMP-activated protein kinase (AMPK) in ECs can be increased by multiple cardiovascular events, we studied the phosphorylation of eNOS Ser633 by AMPK and examined its functional relevance in the mouse models. Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 and eNOS Ser633 phosphorylations, which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. Expression of gain-/loss-of-function eNOS mutants revealed that Ser633 phosphorylation is important for NO production. The aorta of AMPKα2−/− mice showed attenuated atorvastatin-induced eNOS phosphorylation. Nano–liquid chromatography/tandem mass spectrometry (LC/MS/MS) confirmed that eNOS Ser633 was able to compete with Ser1177 or acetyl-coenzyme A carboxylase Ser79 for AMPKα phosphorylation. Nano-LC/MS/MS confirmed that eNOS purified from AICAR-treated ECs was phosphorylated at both Ser633 and Ser1177. Our results indicate that AMPK phosphorylation of eNOS Ser633 is a functional signaling event for NO bioavailability in ECs.