Interactive media server with media synchronized raid storage system

We propose an efficient placement algorithm and per-disk prefetching method to effectively support interactive operations in the media server. Our placement policy is incorporated with an encoder having a special bitcount control scheme that repeatedly tunes quantization parameters to adjust the bitcounts of video frames. This encoder can generate coded frames whose sizes are synchronized with the RAID stripe size, so that when various fast-forward levels are accessed we can reduce the seek and rotational latency and enhance the disk throughput of each disk in the RAID system. In the experimental results, the proposed placement policy and bitrate control scheme can significantly improve the average service time, which can enlarge the capacity of the interactive media server

Understanding the mechanism of glucose-induced relief of Rgt1-mediated repression in yeast

The yeast Rgt1 repressor inhibits transcription of the glucose transporter (HXT) genes in the absence of glucose. It does so by recruiting the general corepressor complex Ssn6-Tup1 and the HXT corepressor Mth1. In the presence of glucose, Rgt1 is phosphorylated by the cAMP-activated protein kinase A (PKA) and dissociates from the HXT promoters, resulting in expression of HXT genes. In this study, using Rgt1 chimeras that bind DNA constitutively, we investigate how glucose regulates Rgt1 function. Our results show that the DNA-bound Rgt1 constructs repress expression of the HXT1 gene in conjunction with Ssn6-Tup1 and Mth1, and that this repression is lifted when they dissociate from Ssn6-Tup1 in high glucose conditions. Mth1 mediates the interaction between the Rgt1 constructs and Ssn6-Tup1, and glucose-induced downregulation of Mth1 enables PKA to phosphorylate the Rgt1 constructs. This phosphorylation induces dissociation of Ssn6-Tup1 from the DNA-bound Rgt1 constructs, resulting in derepression of HXT gene expression. Therefore, Rgt1 removal from DNA occurs in response to glucose but is not necessary for glucose induction of HXT gene expression, suggesting that glucose regulates Rgt1 function by primarily modulating the Rgt1 interaction with Ssn6-Tup1

The Glucose Signaling Network in Yeast

Background Most cells possess a sophisticated mechanism for sensing glucose and responding to it appropriately. Glucose sensing and signaling in the budding yeast Saccharomyces cerevisiae represent an important paradigm for understanding how extracellular signals lead to changes in the gene expression program in eukaryotes. Scope of review This review focuses on the yeast glucose sensing and signaling pathways that operate in a highly regulated and cooperative manner to bring about glucose-induction of HXT gene expression. Major conclusions The yeast cells possess a family of glucose transporters (HXTs), with different kinetic properties. They employ three major glucose signaling pathways—Rgt2/Snf3, AMPK, and cAMP-PKA—to express only those transporters best suited for the amounts of glucose available. We discuss the current understanding of how these pathways are integrated into a regulatory network to ensure efficient uptake and utilization of glucose. General significance Elucidating the role of multiple glucose signals and pathways involved inglucose uptake and metabolism in yeast may reveal the molecular basis of glucose homeostasis in humans, especially under pathological conditions, such as hyperglycemia in diabetics and the elevated rate of glycolysis observed in many solid tumors

Assessing Glucose Uptake through the Yeast Hexose Transporter 1 (Hxt1)

The transport of glucose across the plasma membrane is mediated by members of the glucose transporter family. In this study, we investigated glucose uptake through the yeast hexose transporter 1 (Hxt1) by measuring incorporation of 2-NBDG, a non-metabolizable, fluorescent glucose analog, into the yeast Saccharomyces cerevisiae. We find that 2-NBDG is not incorporated into the hxt null strain lacking all glucose transporter genes and that this defect is rescued by expression of wild type Hxt1, but not of Hxt1 with mutations at the putative glucose-binding residues, inferred from the alignment of yeast and human glucose transporter sequences. Similarly, the growth defect of the hxt null strain on glucose is fully complemented by expression of wild type Hxt1, but not of the mutant Hxt1 proteins. Thus, 2-NBDG, like glucose, is likely to be transported into the yeast cells through the glucose transport system. Hxt1 is internalized and targeted to the vacuole for degradation in response to glucose starvation. Among the mutant Hxt1 proteins, Hxt1N370A and HXT1W473A are resistant to such degradation. Hxt1N370A, in particular, is able to neither uptake 2-NBDG nor restore the growth defect of the hxt null strain on glucose. These results demonstrate 2-NBDG as a fluorescent probe for glucose uptake in the yeast cells and identify N370 as a critical residue for the stability and function of Hxt1

Mth1 regulates the interaction between the Rgt1 repressor and the Ssn6-Tup1 corepressor complex by modulating PKA-dependent phosphorylation of Rgt1

Glucose uptake, the first, rate-limiting step of its utilization, is facilitated by glucose transporters. Expression of several glucose transporter (HXT) genes in yeast is repressed by the Rgt1 repressor, which recruits the glucose-responsive transcription factor Mth1 and the general corepressor complex Ssn6-Tup1 in the absence of glucose; however, it is derepressed when Mth1 is inactivated by glucose. Here we show that Ssn6-Tup1 interferes with the DNA-binding ability of Rgt1 in the absence of Mth1 and that the Rgt1 function abrogated by Ssn6 overexpression is restored by co-overexpression of Mth1. Thus Mth1 likely regulates Rgt1 function not by modulating its DNA-binding activity directly but by functionally antagonizing Ssn6-Tup1. Mth1 does so by acting as a scaffold-like protein to recruit Ssn6-Tup1 to Rgt1. Supporting evidence shows that Mth1 blocks the protein kinase A–dependent phosphorylation of Rgt1 that impairs the ability of Rgt1 to interact with Ssn6-Tup1. Of note, Rgt1 can bind DNA in the absence of Ssn6-Tup1 but does not inhibit transcription, suggesting that dissociation of Rgt1 from Ssn6-Tup1, but not from DNA, is necessary and sufficient for the expression of its target genes. Taken together, these findings show that Mth1 is a transcriptional corepressor that facilitates the recruitment of Ssn6-Tup1 by Rgt1

Isolation of p-hydroxycinnamaldehyde as an antibacterial substance from the saw fly, Acantholyda parki S.

AbstractWe purified an antibacterial substance from larvae of the saw fly, Acantholyda parki S., and identified its molecular structure as p-hydroxycinnamaldehyde. We then synthesized it by reduction of p-hydroxycinnamic acid. The antibacterial activity of the synthetic p-hydroxycinnamaldehyde was equal to that of the authentic substance. This molecule was found to have a broad antibacterial spectrum against not only Gram-negative, but also Gram-positive bacteria. Furthermore, it showed antifungal activity against Candida albicans. We suggest that this substance may play a role in the defense system of this insect. This is the first report of p-hydroxycinnamaldehyde of animal origin

Bioinspired reversible hydrogel adhesives for wet and underwater surfaces

Stable and reversible adhesion to wet surfaces is challenging owing to water molecules at the contact interface. In this study, we develop a hydrogel-based wet adhesive, which can exhibit strong and reversible adhesion to wet and underwater surfaces as well as to dry surfaces. The remarkable wet adhesion of the hydrogel adhesive is realized based on a synergetic integration of bioinspired microarchitectures and water-friendly and water-absorbing properties of the polymeric hydrogel. Under dry conditions, the microstructured hydrogel adhesive exhibits strong van der Waals interaction-based adhesion, while under underwater conditions, it can maximize capillary adhesion. Consequently, the hydrogel adhesive exhibits remarkable adhesion strengths for dry, moist, and submerged substrates. Maximum normal and shear adhesion strengths of 423 and 384, 492 and 340, and 253 and 21 kPa are achieved with the hydrogel adhesive for dry, moist, and submerged substrates, respectively. Our results demonstrate that strong wet and underwater adhesion can be achieved only with the hydrogel-based adhesive with simple microscale architecture