A single synaptic device with inherent learning and memory functions is demonstrated based on an amorphous InGaZnO (α‐IGZO) memristor; several essential synaptic functions are simultaneously achieved in such a single device, including nonlinear transmission characteristics, spike‐rate‐dependent and spike‐timing‐dependent plasticity, long‐term/short‐term plasticity (LSP and STP) and “learning‐experience” behavior. These characteristics bear striking resemblances to certain learning and memory functions of biological systems. Especially, a “learning‐experience” function is obtained for the first time, which is thought to be related to the metastable local structures in α‐IGZO. These functions are interrelated: frequent stimulation can cause an enhancement of LTP, both spike‐rate‐dependent and spike‐timing‐dependent plasticity is the same on this point; and, the STP‐to‐LTP transition can occur through repeated “stimulation” training. The physical mechanism of device operation, which does not strictly follow the memristor model, is attributed to oxygen ion migration/diffusion. A correlation between short‐term memory and ion diffusion is established by studying the temperature dependence of the relaxation processes of STP and ion diffusion. The realization of important synaptic functions and the establishment of a dynamic model would promote more accurate modeling of the synapse for artificial neural network.

Netrins regulate axon path-finding during development, but the underlying mechanisms are not well understood. Here, we provide evidence for the involvement of the unconventional myosin X (Myo X) in netrin-1 function. We find that Myo X interacts with the netrin receptor deleted in colorectal cancer (DCC) and neogenin, a DCC-related protein. Expression of Myo X redistributes DCC to the cell periphery or to the tips of neurites, whereas its silencing prevents DCC distribution in neurites. Moreover, expression of DCC, but not neogenin, stimulates Myo X-mediated formation and elongation of filopodia, suggesting that Myo X function may be differentially regulated by DCC and neogenin. The involvement of Myo X in netrin-1 function was further supported by the effects of inhibiting Myo X function in neurons. Cortical explants derived from mouse embryos expressing a motor-less Myo X exhibit reduced neurite outgrowth in response to netrin-1 and chick commissural neurons expressing the motor-less Myo X, or in which Myo X is silenced using microRNA (miRNA), show impaired axon projection in vivo. Taken together, these results identify a novel role for Myo X in regulating netrin-1 function.

Increased transcriptional complex activity, or pharmacological mimics of increased complex activity, predict lifespan in mice and mediate the protective effects of dietary restriction during aging.

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Background:Myosin X (MYO10) was recently reported to promote tumour invasion by transporting integrins to filopodial tips in breast cancer. However, the role of MYO10 in tumours remains poorly defined. Here, we report that MYO10 is required in invadopodia to mediate invasive growth and extracellular matrix degradation, which depends on the binding of MYO10's pleckstrin homology domain to PtdIns(3,4,5)P3.Methods:The expression of MYO10 and its associations with clinicopathological and biological factors were examined in breast cancer cells and breast cancer specimens (n=120). Cell migration and invasion were investigated after the silencing of MYO10. The ability of cells to form invadopodia was studied using a fluorescein isothiocyanate-conjugated gelatin degradation assay. A mouse model was established to study tumour invasive growth and metastasis in vivo.Results:Elevated MYO10 levels were correlated with oestrogen receptor status, progesterone receptor status, poor differentiation, and lymph node metastasis. Silencing MYO10 reduced cell migration and invasion. Invadopodia were responsible for MYO10's role in promoting invasion. Furthermore, decreased invasive growth and lung metastasis were observed in the MYO10-silenced nude mouse model.Conclusions:Our findings suggest that elevated MYO10 expression increases the aggressiveness of breast cancer; this effect is dependent on the involvement of MYO10 in invadopodial formation.

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