| Abstract: |
SYT-SSX protein, resulted from chromosomal translocation, causes synovial sarcoma, which is a malignant tumor accounting for 10% of soft tissue sarcoma. However, biological functions of SYT (synovial sarcoma translocation), also known as SS18, are largely unclear, whereas it has been proven that Syt-null mice die at early stages of embryonic development. Here, we generated Syt-deficient mice and confirmed the reported phenotypes, including growth retardation, open neural tube and haplo-insufficient lethality, and therefore, there is no doubt that Syt is essential for embryonic development. However, placental defects, described in the earlier report, were rarely seen in our mice and we frequently observed cardiac defect in Syt-deficient mice. As the mechanisms responsible for embryonic lethality seem to be complicate, we performed additional experiments. By using primary cultured embryonic fibroblasts, we showed that Syt / MEFs deregulate actin organization and suppressed cell migration. These observations suggest that Syt may contribute to the signaling pathway important for various cellular functions in vivo and in vitro, and we propose that Syt-deficient MEFs would be a powerful means to understand the biological roles of SYT in vitro. © 2009 USCAP, Inc. All rights reserved. |
| Keywords: |
signal transduction; controlled study; proto-oncogene proteins; nonhuman; animal cell; mouse; phenotype; animals; mice; mice, knockout; actin; animal tissue; cells, cultured; cell function; proto oncogene; embryo; animal experiment; animal model; embryo development; in vivo study; in vitro study; regulatory mechanism; nucleotide sequence; newborn; cell migration; fibroblast; fibroblasts; cell movement; organization; embryo, mammalian; pregnancy; protein deficiency; animals, newborn; synovial sarcoma; actins; repressor proteins; cardiogenesis; embryonic lethality; motility; p300; syt; synaptotagmin; congenital heart malformation; fibroblast culture; growth retardation; knockout mouse; lethality; migration inhibition; neural tube; placenta disorder; synovial sarcoma translocation gene; embryo loss; embryonic development; heart defects, congenital; placenta
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