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研究発表を行った学会；
・第４０回日本発生生物学会・第５９回日本細胞生物学会　合同大会、2007年 5月28~30日(福岡)

タイトル；Studies on the function of Sall4 upon mouse germ cell development.
発表者；　山口　泰華　氏
　　　（熊本大学　発生医学研究センター　細胞識別分野）
Abstract；
Sall4 is a mouse homolog of the Zn-finger transcriptional factor, Drosophila Spalt gene. We previously demonstrated that conventional Sall4 null mutant embryos died shortly after the implantation may due to the impaired proliferation of the inner cell mass derived cells. Consistent with this, Sall4-null ES cells, which avoid the function of both Sall4 alleles showed the deficient in their proliferation, whereas the loss of Sall4 function seemed to be not affected on Pou5f1 (Oct-3/4) expression (Yumoto-Sakaki et al., 2006). Recently, it has been shown that Sall4 interacts with either Pou5f1 or Nanog, and proposed the potential Sall4 function in ES cell self-renewal and/or differentiation.
By the detail expression analysis of Sall4 in developing mouse embryos, we found that Sall4 protein is expressed in migratory and gonadal primordial germ cells (PGCs), and is localized to the hetero-chromatin region in nucleus. Therefore, we generated two kinds of Sall4 conditional knockout (CKO) mice, CKO specifically in the epiblast using SOX2-Cre and CKO specifically in the PGCs using the TNAP-Cre, to examine effects of Sall4 on the germ cell development at the two different developmental stages. Sall4 SOX2-Cre CKO embryos could form PGCs but showed defects in the relocation of PGCs from the embryonic mesoderm to the endoderm at the early-head-fold-stage. On the other hand, Sall4 TNAP-Cre CKO embryos showed the reduction of the number of Ddx4/mvh positive PGCs in the fetal gonad. We discuss the potential Sall4 function in the mouse germ cell development.