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Maternal effect genes play critical roles in early embryogenesis of model organisms where they have been intensively investigated. However, their molecular function in mammals remains largely unknown. Recently, we identified a subcortical maternal complex (SCMC) that contains four proteins encoded by maternal effect genes (Mater, Filia, Floped and Tle6). Here we report that TLE6, similar to FLOPED and MATER, stabilizes the SCMC and is necessary for cleavage beyond the two-cell stage of development. We document that the SCMC is required for formation of the cytoplasmic F-actin meshwork that controls the central position of the spindle and ensures symmetric division of mouse zygotes. We further demonstrate that the SCMC controls formation of the actin cytoskeleton specifically via Cofilin, a key regulator of F-actin assembly. Our results provide molecular insight into the physiological function of TLE6, its interaction with the SCMC and their roles in the symmetric division of the zygote in early mouse development.

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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.

In this paper, 550 h ͑500 h continuous and 50 h intermittent͒ high-temperature proton exchange membrane fuel cell ͑PEMFC, phosphoric acid-doped polybenzimidazole system, H 3 PO 4 /PBI͒ life test was performed without humidification at 150°C; constant current ͑at 640 mA cm −2 ͒ performance and polarization curves were recorded. Electrochemical and physical characterizations were applied to investigate the degradation of the membrane electrode assembly ͑MEA͒. The results showed that the constant current performance started to reduce with a rate of 0.18 mV h −1 after about 90 h activation. Surface area loss of the cathode platinum due to agglomeration was detected by cyclic voltammetry and transmission electron microscopy. A slight increase of internal resistance of the single cell due to H 3 PO 4 leaching was found by electrochemical impedance spectroscopy and energy dispersive X-ray analysis. H 2 permeability of MEA increased during the last 50 h intermittent test because of appearing of cracks, that were detected by linear sweep voltammetry and scanning electron microscopy. These results suggested that catalyst agglomeration and H 3 PO 4 leaching from catalyst layers contributed to the performance degradation of the MEA during the life test, and mechanical properties degradation of H 3 PO 4 /PBI membrane impacted badly the lifetime of the single cell.

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Contaminants were selected from the Environmental Protection Agency lists. Six qualitative down selection criteria were used to reduce the list to the 21 1 st tier contaminants. The effect of 1 st tier contaminants, mostly organic with the exception of ozone, on PEMFC performance is reported. The behavior of these contaminants was classified into 5 different cases; no effect, recoverable effect, partly recoverable effect, irrecoverable effect and supra-recoverable effect. The steady state contamination and irrecoverable performance losses respectively varied from 0 to 90% and −2 to 80%. Contamination and recovery time scales significantly varied within a ∼0.01 to ∼28 h range. Acetaldehyde and propene were characterized by the new supra-recoverable effect. For trichlorofluoromethane, iso-propanol and propene, a decrease of the relative humidity led to a significant change in cell performance (steady states, time scales). This effect was ascribed to several causes including the scavenging effect of liquid water by contaminant dissolution and a non zero water reaction order. Two quantitative selection criteria based on observed fuel cell performance were used to reduce the 1 st tier list to 7 2 nd tier contaminants for more resource intensive tests. These 2 nd tier contaminants are acetonitrile, acetylene, bromomethane, iso-propanol, methyl methacrylate, naphthalene and propene.

The effects of trace concentrations of SO2 contaminant present in the cathode feed stream on proton exchange membrane fuel cell (PEMFC) performance are studied. Contaminant concentrations of 1, 2, and 10 ppm were exposed to the cell applying a total dosage of 160μmol of SO2 at 80°C and a current density of 0.6Acm−2 . All experiments show significant cell performance degradation before the steady-state poisoning state is reached. The performance degradation shows an inflection in the cell voltage, which is attributed to at least two different poisoning processes. The overall poisoning process is shown to consist of an irreversible part and a reversible part. While the performance loss of the reversible part is dependent on the SO2 concentration and is recoverable during a normalH2/air operation, that of the irreversible part is greatly recoverable by potential cycling in the normalH2/normalN2 mode. Evidence is also presented that cathode exposure to SO2 results in a performance impact at the anode. Furthermore, sulfur species that remain in the membrane electrode assembly accelerate the cell performance degradation during a neat normalH2/air operation and subsequent SO2 contaminant exposure.