968 resultados para ARM


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Single core capabilities have reached their maximum clock speed; new multicore architectures provide an alternative way to tackle this issue instead. The design of decoding applications running on top of these multicore platforms and their optimization to exploit all system computational power is crucial to obtain best results. Since the development at the integration level of printed circuit boards are increasingly difficult to optimize due to physical constraints and the inherent increase in power consumption, development of multiprocessor architectures is becoming the new Holy Grail. In this sense, it is crucial to develop applications that can run on the new multi-core architectures and find out distributions to maximize the potential use of the system. Today most of commercial electronic devices, available in the market, are composed of embedded systems. These devices incorporate recently multi-core processors. Task management onto multiple core/processors is not a trivial issue, and a good task/actor scheduling can yield to significant improvements in terms of efficiency gains and also processor power consumption. Scheduling of data flows between the actors that implement the applications aims to harness multi-core architectures to more types of applications, with an explicit expression of parallelism into the application. On the other hand, the recent development of the MPEG Reconfigurable Video Coding (RVC) standard allows the reconfiguration of the video decoders. RVC is a flexible standard compatible with MPEG developed codecs, making it the ideal tool to integrate into the new multimedia terminals to decode video sequences. With the new versions of the Open RVC-CAL Compiler (Orcc), a static mapping of the actors that implement the functionality of the application can be done once the application executable has been generated. This static mapping must be done for each of the different cores available on the working platform. It has been chosen an embedded system with a processor with two ARMv7 cores. This platform allows us to obtain the desired tests, get as much improvement results from the execution on a single core, and contrast both with a PC-based multiprocessor system. Las posibilidades ofrecidas por el aumento de la velocidad de la frecuencia de reloj de sistemas de un solo procesador están siendo agotadas. Las nuevas arquitecturas multiprocesador proporcionan una vía de desarrollo alternativa en este sentido. El diseño y optimización de aplicaciones de descodificación de video que se ejecuten sobre las nuevas arquitecturas permiten un mejor aprovechamiento y favorecen la obtención de mayores rendimientos. Hoy en día muchos de los dispositivos comerciales que se están lanzando al mercado están integrados por sistemas embebidos, que recientemente están basados en arquitecturas multinúcleo. El manejo de las tareas de ejecución sobre este tipo de arquitecturas no es una tarea trivial, y una buena planificación de los actores que implementan las funcionalidades puede proporcionar importantes mejoras en términos de eficiencia en el uso de la capacidad de los procesadores y, por ende, del consumo de energía. Por otro lado, el reciente desarrollo del estándar de Codificación de Video Reconfigurable (RVC), permite la reconfiguración de los descodificadores de video. RVC es un estándar flexible y compatible con anteriores codecs desarrollados por MPEG. Esto hace de RVC el estándar ideal para ser incorporado en los nuevos terminales multimedia que se están comercializando. Con el desarrollo de las nuevas versiones del compilador específico para el desarrollo de lenguaje RVC-CAL (Orcc), en el que se basa MPEG RVC, el mapeo estático, para entornos basados en multiprocesador, de los actores que integran un descodificador es posible. Se ha elegido un sistema embebido con un procesador con dos núcleos ARMv7. Esta plataforma nos permitirá llevar a cabo las pruebas de verificación y contraste de los conceptos estudiados en este trabajo, en el sentido del desarrollo de descodificadores de video basados en MPEG RVC y del estudio de la planificación y mapeo estático de los mismos.

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The chromosomal DNA of the bacteria Streptomyces ambofaciens DSM40697 is an 8-Mb linear molecule that ends in terminal inverted repeats (TIRs) of 210 kb. The sequences of the TIRs are highly variable between the different linear replicons of Streptomyces (plasmids or chromosomes). Two spontaneous mutant strains harboring TIRs of 480 and 850 kb were isolated. The TIR polymorphism seen is a result of the deletion of one chromosomal end and its replacement by 480 or 850 kb of sequence identical to the end of the undeleted chromosomal arm. Analysis of the wild-type sequences involved in these rearrangements revealed that a recombination event took place between the two copies of a duplicated DNA sequence. Each copy was mapped to one chromosomal arm, outside of the TIR, and encoded a putative alternative sigma factor. The two ORFs, designated hasR and hasL, were found to be 99% similar at the nucleotide level. The sequence of the chimeric regions generated by the recombination showed that the chromosomal structure of the mutant strains resulted from homologous recombination events between the two copies. We suggest that this mechanism of chromosomal arm replacement contributes to the rapid evolutionary diversification of the sequences of the TIR in Streptomyces.

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Tctex2 is thought to be one of the distorter genes of the mouse t haplotype. This complex greatly biases the segregation of the chromosome that carries it such that in heterozygous +/t males, the t haplotype is transmitted to >95% of the offspring, a phenomenon known as transmission ratio distortion. The LC2 outer dynein arm light chain of Chlamydomonas reinhardtii is a homologue of the mouse protein Tctex2. We have identified Chlamydomonas insertional mutants with deletions in the gene encoding LC2 and demonstrate that the LC2 gene is the same as the ODA12 gene, the product of which had not been identified previously. Complete deletion of the LC2/ODA12 gene causes loss of all outer arms and a slow jerky swimming phenotype. Transformation of the deletion mutant with the cloned LC2/ODA12 gene restores the outer arms and rescues the motility phenotype. Therefore, LC2 is required for outer arm assembly. The fact that LC2 is an essential subunit of flagellar outer dynein arms allows us to propose a detailed mechanism whereby transmission ratio distortion is explained by the differential binding of mutant (t haplotype encoded) and wild-type dyneins to the axonemal microtubules of t-bearing or wild-type sperm, with resulting differences in their motility.

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Previous structural and biochemical studies have revealed that the inner arm dynein I1 is targeted and anchored to a unique site located proximal to the first radial spoke in each 96-nm axoneme repeat on flagellar doublet microtubules. To determine whether intermediate chains mediate the positioning and docking of dynein complexes, we cloned and characterized the 140-kDa intermediate chain (IC140) of the I1 complex. Sequence and secondary structural analysis, with particular emphasis on β-sheet organization, predicted that IC140 contains seven WD repeats. Reexamination of other members of the dynein intermediate chain family of WD proteins indicated that these polypeptides also bear seven WD/β-sheet repeats arranged in the same pattern along each intermediate chain protein. A polyclonal antibody was raised against a 53-kDa fusion protein derived from the C-terminal third of IC140. The antibody is highly specific for IC140 and does not bind to other dynein intermediate chains or proteins in Chlamydomonas flagella. Immunofluorescent microscopy of Chlamydomonas cells confirmed that IC140 is distributed along the length of both flagellar axonemes. In vitro reconstitution experiments demonstrated that the 53-kDa C-terminal fusion protein binds specifically to axonemes lacking the I1 complex. Chemical cross-linking indicated that IC140 is closely associated with a second intermediate chain in the I1 complex. These data suggest that IC140 contains domains responsible for the assembly and docking of the I1 complex to the doublet microtubule cargo.

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To identify new loci that are involved in the assembly and targeting of dynein complexes, we have screened a collection of motility mutants that were generated by insertional mutagenesis. One such mutant, 5B10, lacks the inner arm isoform known as the I1 complex. This isoform is located proximal to the first radial spoke in each 96-nm axoneme repeat and is an important target for the regulation of flagellar motility. Complementation tests reveal that 5B10 represents a new I1 locus, IDA7. Biochemical analyses confirm that ida7 axonemes lack at least five I1 complex subunits. Southern blots probed with a clone containing the gene encoding the 140-kDa intermediate chain (IC) indicate that the ida7 mutation is the result of plasmid insertion into the IC140 gene. Transformation with a wild-type copy of the IC140 gene completely rescues the mutant defects. Surprisingly, transformation with a construct of the IC140 gene lacking the first four exons of the coding sequence also rescues the mutant phenotype. These studies indicate that IC140 is essential for assembly of the I1 complex, but unlike other dynein ICs, the N-terminal region is not critical for its activity.

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The myosin head consists of a globular catalytic domain that binds actin and hydrolyzes ATP and a neck domain that consists of essential and regulatory light chains bound to a long alpha-helical portion of the heavy chain. The swinging neck-level model assumes that a swinging motion of the neck relative to the catalytic domain is the origin of movement. This model predicts that the step size, and consequently the sliding velocity, are linearly related to the length of the neck. We have tested this point by characterizing a series of mutant Dictyostelium myosins that have different neck lengths. The 2xELCBS mutant has an extra binding site for essential light chain. The delta RLCBS mutant myosin has an internal deletion that removes the regulatory light chain binding site. The delta BLCBS mutant lacks both light chain binding sites. Wild-type myosin and these mutant myosins were subjected to the sliding filament in vitro motility assay. As expected, mutants with shorter necks move slower than wild-type myosin in vitro. Most significantly, a mutant with a longer neck moves faster than the wild type, and the sliding velocities of these myosins are linearly related to the neck length, as predicted by the swinging neck-lever model. A simple extrapolation to zero speed predicts that the fulcrum point is in the vicinity of the SH1-SH2 region in the catalytic domain.