Seongsoo Lee

Intra-task voltage scheduling for low-energy hard real-time applications

A novel intra-task voltage-scheduling algorithm controls the supply voltage within an individual task boundary. By fully exploiting slack time, it achieves a high-energy reduction ratio. Using this algorithm, a software tool automatically converts an application into a low energy version.

Low-energy intra-task voltage scheduling using static timing analysis

We propose an intra-task voltage scheduling algorithm for low-energy hard real-time applications. Based on a static timing analysis technique, the proposed algorithm controls the supply voltage within an individual task boundary. By fully exploiting all the slack times, a scheduled program by the proposed algorithm always complete its execution near the deadline, thus achieving a high energy reduction ratio. In order to validate the effectiveness of the proposed algorithm, we built a software tool that automatically converts a DVS-unaware program into an equivalent low-energy program. Experimental results show that the low-energy version of an MPEG-4 encoder/decoder (converted by the software tool) consumes less than 7

The F-actin-microtubule crosslinker Shot is a platform for Krasavietz-mediated translational regulation of midline axon repulsion.

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New motion estimation algorithm using adaptively quantized low bit-resolution image and its VLSI architecture for MPEG2 video encoding

25% of the original program running on a fixed-voltage system with a power-down mode.

dCIP4 (Drosophila Cdc42-Interacting Protein 4) Restrains Synaptic Growth by Inhibiting the Secretion of the Retrograde Glass Bottom Boat Signal

Axon extension and guidance require a coordinated assembly of F-actin and microtubules as well as regulated translation. The molecular basis of how the translation of mRNAs encoding guidance proteins could be closely tied to the pace of cytoskeletal assembly is poorly understood. Previous studies have shown that the F-actin-microtubule crosslinker Short stop (Shot) is required for motor and sensory axon extension in the Drosophila embryo. Here, we provide biochemical and genetic evidence that Shot functions with a novel translation inhibitor, Krasavietz (Kra, Exba), to steer longitudinally directed CNS axons away from the midline. Kra binds directly to the C-terminus of Shot, and this interaction is required for the activity of Shot to support midline axon repulsion. shot and kra mutations lead to weak robo-like phenotypes, and synergistically affect midline avoidance of CNS axons. We also show that shot and kra dominantly enhance the frequency of midline crossovers in embryos heterozygous for slit or robo, and that in kra mutant embryos, some Robo-positive axons ectopically cross the midline that normally expresses the repellent Slit. Finally, we demonstrate that Kra also interacts with the translation initiation factor eIF2β and inhibits translation in vitro. Together, these data suggest that Kra-mediated translational regulation plays important roles in midline axon repulsion and that Shot functions as a direct physical link between translational regulation and cytoskeleton reorganization.

Imbalance of mitochondrial dynamics in Drosophila models of amyotrophic lateral sclerosis

This paper describes a new motion estimation algorithm that is suitable for hardware implementation and substantially reduces the hardware cost by using a low bit-resolution image in the block matching. In the low bit-resolution image generation, adaptive quantization is employed to reduce the bit resolution of the pixel values, which is better than simple truncation of the least significant bits in preserving the dynamic range of the pixel values. The proposed algorithm consists of two search steps: in the low-resolution search, a set of candidate motion vectors is determined, and in the full-resolution search, the motion vector is found from these candidate motion vectors. The hardware cost of the proposed algorithm is 1/17 times of the full search algorithm, while its peak signal-to-noise ratio is better than that of the 4:1 alternate subsampling for the search range of /spl plusmn/32/spl times//spl plusmn/32. A VLSI architecture of the proposed algorithm is also described, which can concurrently perform two prediction modes of the MPEG2 video standard with the search range of (-32.0,-32.0)-(+31.5,+31.5). We fabricated a MPEG2 motion estimator with a 0.5-/spl mu/m triple-metal CMOS technology. The VLSI chip includes 110 K gates of random logic and 90 K bits of SRAM in a die size of 11.5 mm/spl times/12.5 mm. The full functionality of the fabricated chip was confirmed with an MPEG2 encoder chip.

Two-step motion estimation algorithm using low-resolution quantization

The bone morphogenetic protein (BMP) ligand Glass bottom boat (Gbb) acts as a retrograde growth signal at the Drosophila neuromuscular junction (NMJ). Endocytic regulation of presynaptic BMP receptors has been proposed to attenuate retrograde BMP signaling. However, it remains unknown whether the Gbb signal is also regulated by postsynaptic mechanisms. Here, we provide evidence that Drosophila Cdc42-interacting protein 4 (dCIP4) functions postsynaptically to inhibit synaptic growth. dCIP4 is localized postsynaptically at NMJs. dcip4 mutations lead to synaptic overgrowth and increased presynaptic phosphorylated mothers against decapentaplegic (Mad) levels, and these defects are rescued by muscle-specific expression of dCIP4. Biochemical and genetic analyses demonstrate that dCIP4 acts downstream of Cdc42 to activate the postsynaptic Wsp–Arp2/3 pathway. We also show that BMP signaling is necessary for synaptic overgrowth in larvae lacking postsynaptic dcip4 or wsp. Finally, dCIP4 and Wsp inhibit Gbb secretion. Thus, we propose that dCIP4 restrains synaptic growth by inhibiting postsynaptic Gbb secretion through the Wsp–Arp2/3 pathway.

Neuroprotective Effects of Protein Tyrosine Phosphatase 1B Inhibition against ER Stress-Induced Toxicity

Amyotrophic lateral sclerosis (ALS) is the most common neurodegenerative disease, characterized by progressive and selective loss of motor neurons in the brain and spinal cord. DNA/RNA-binding proteins such as TDP-43, FUS, and TAF15 have been linked with the sporadic and familial forms of ALS. However, the exact pathogenic mechanism of ALS is still unknown. Recently, we found that ALS-causing genes such as TDP-43, FUS, and TAF15 genetically interact with mitochondrial dynamics regulatory genes. In this study, we show that mitochondrial fission was highly enhanced in muscles and motor neurons of TDP-43, FUS, and TAF15-induced fly models of ALS. Furthermore, the mitochondrial fission defects were rescued by co-expression of mitochondrial dynamics regulatory genes such as Marf, Opa1, and the dominant negative mutant form of Drp1. Moreover, we found that the expression level of Marf was decreased in ALS-induced flies. These results indicate that the imbalance of mitochondrial dynamics caused by instability of Marf is linked to the pathogenesis of TDP-43, FUS, and TAF15-associated ALS.

Protective effect of Drosophila glutathione transferase omega 1 against hydrogen peroxide-induced neuronal toxicity

We propose a new motion estimation algorithm using low-resolution quantization. The proposed algorithm reduces both performance degradation and computational cost by matching at every search position with a low bit resolution image. It consists of two steps: the low resolution search that generates the candidate motion vectors and the full-resolution search that finds the best motion vector in the candidates from the low-resolution search. Simulation results show that the PSNR of the proposed algorithm is superior to that of the 4:1 alternate subsampling algorithm and the one-dimensional full search algorithm with less computational cost. The PSNR degradation of the proposed algorithm with respect to the full search algorithm is less than 0.12 dB with 1/17.7 computational cost.

The phosphoinositide phosphatase Sac1 is required for midline axon guidance

Several lines of evidence suggest that endoplasmic reticulum (ER) stress plays a critical role in the pathogenesis of many neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Protein tyrosine phosphatase 1B (PTP1B) is known to regulate the ER stress signaling pathway, but its role in neuronal systems in terms of ER stress remains largely unknown. Here, we showed that rotenone-induced toxicity in human neuroblastoma cell lines and mouse primary cortical neurons was ameliorated by PTP1B inhibition. Moreover, the increase in the level of ER stress markers (eIF2α phosphorylation and PERK phosphorylation) induced by rotenone treatment was obviously suppressed by concomitant PTP1B inhibition. However, the rotenone-induced production of reactive oxygen species (ROS) was not affected by PTP1B inhibition, suggesting that the neuroprotective effect of the PTP1B inhibitor is not associated with ROS production. Moreover, we found that MG132-induced toxicity involving proteasome inhibition was also ameliorated by PTP1B inhibition in a human neuroblastoma cell line and mouse primary cortical neurons. Consistently, downregulation of the PTP1B homologue gene in Drosophila mitigated rotenone- and MG132-induced toxicity. Taken together, these findings indicate that PTP1B inhibition may represent a novel therapeutic approach for ER stress-mediated neurodegenerative diseases.