The assembly of striated muscle myofibrils is a multistep process in which a variety of proteins is involved. One of the first and most important steps in myofibrillogenesis is the arrangement of thin myofilaments into ordered I-Z-I brushes, requiring the coordinated activity of numerous actin binding proteins. The early expression of myopodin prior to sarcomeric α-actinin, as well as its binding to actin, α-actinin and filamin indicate an important role for this protein in actin cytoskeleton remodelling with the precise function of myopodin in this process yet remaining to be resolved. While myopodin was previously described as a protein capable of cross-linking actin filaments into thick bundles upon transient transfections, it has remained unclear whether myopodin alone is capable of bundling actin, or if additional proteins are involved. We have therefore investigated the in vitro actin binding properties of myopodin. High speed cosedimentation assays with skeletal muscle actin confirmed direct binding of myopodin to F-actin and showed that this interaction is mediated by at least two independent actin binding sites, found in all myopodin isoforms identified to date. Furthermore, low-speed cosedimentation assays revealed that not only full length myopodin, but also the fragment containing only the second binding site, bundles microfilaments in the absence of accessory proteins. Ultrastructural analysis demonstrated that this bundling activity resembled that of α-actinin. Biochemical experiments revealed that bundling was not achieved by myopodin's ability to dimerize, indicating the presence of two individual F-actin binding sites within the second binding segment. Thus full length myopodin contains at least three F-actin binding sites. These data provide further understanding of the mechanisms by which myopodin contributes to actin reorganization during myofibril assembly.
Reducing component size and increasing the operating frequency of integrated circuits makes the Systems-on-Chip (SoCs) more susceptible to faults. Faults can cause errors, and errors can be propagated and lead to a system failure. SoCs employing many cores rely on a Network-on-Chip (NoC) as the interconnect architecture. In this context, this study explores alternatives to implement the flow regulation, routing, and arbitration controllers of an NoC router aiming at minimizing error propagation. For this purpose, a router with Finite-State Machine (FSM)-based controllers was developed targeting low use of logical resources and design flexibility for implementation in FPGA devices. We elaborated and compared the synthesis and simulation results of architectures that vary their controllers on Moore and Mealy FSMs, as well as the Triple Modular Redundancy (TMR) hardening application. Experimental results showed that the routing controller was the most critical one and that migrating a Moore to a Mealy controller offered a lower error propagation rate and higher performance than the application of TMR. We intended to use the proposed router architecture to integrate cores in a fault-tolerant NoC-based system for data processing in harsh environments, such as in space applications.
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