SUMMARYControlled delivery of myofibril components to the appropriate sites of assembly is crucial for myofibrillogenesis. Here, we show that kinesin-1 heavy chain Kif5b plays important roles in anterograde transport of -sarcomeric actin, non-muscle myosin IIB, together with intermediate filament proteins desmin and nestin to the growing tips of the elongating myotubes. Mice with Kif5b conditionally knocked out in myogenic cells showed aggregation of actin filaments and intermediate filament proteins in the differentiating skeletal muscle cells, which further affected myofibril assembly and their linkage to the myotendinous junctions. The expression of Kif5b in mutant myotubes rescued the localization of the affected proteins. Functional mapping of Kif5b revealed a 64-amino acid -helix domain in the tail region, which directly interacted with desmin and might be responsible for the transportation of these proteins in a complex.

Background The growth plate is a special region of the cartilage that drives longitudinal growth of long bones. Proliferating chondrocytes in the growth plate, arranged in columns, divide perpendicular to the long axis of the growth plate then intercalate to re-align with parental columns. Which molecular partners maintain growth plate columnar structures and chondrocyte cytokinesis has not been fully revealed. It is reported that kinesin family member 3A (KIF3A), a subunit of kinesin-2, plays an important role in maintaining columnar organization in growth plates via controlling primary cilia formation and cell proliferation. Result Here we identify kinesin family member 5B (KIF5B), the heavy chain of kinesin-1, a ubiquitously expressed motor protein for anterograde intracellular transport along the microtubule network, as a key modulator of cytokinesis in chondrocytes via maintenance of central spindle organization. We show that KIF5B is concentrated in the central spindle during cytokinesis in both primary chondrocytes and chondrogenic ATDC5 cells. Conclusion The failure of cytokinesis in KIF5B null chondrocytes leads to incomplete cell rotation, disrupting proliferation and differentiation, and results in a disorganized growth plate.

Future mobile wireless communication networks will be featured as heterogeneity in order to enhance network performance and improve user experience. For better adaption to network challenges over its complexity and vulnerability, cell outage detection technique, a promising intelligent part of selforganizing networks (SON), has drawn considerable attention to deal with unexpected network faults. Our work is devoted to cell outage detection in a two-tier macro-pico network. Based on observation of performance metrics in time domain, we employ a classification algorithm called K-nearest neighbor (KNN) to achieve automatic anomaly detection. With some reasonable assumptions and a LTE-A system simulator, numerical experiments are implemented to demonstrate the efficiency of the proposed algorithm. Finally, localization for anomaly data and performance evaluation are further carried out to validate the classification accuracy.