アクティブボード・２０１２年　８月
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研究発表を行った学会；
・第４５回日本発生生物学会
　２０１２年　５月２８日〜３１日（神戸）

タイトル；Six1 and Six4 homeodomain proteins act downstream to BMP signal in mouse primordial germ cell formation.

発表者；田中　聡　氏
　　　（熊本大学　発生医学研究所　腎臓発生分野）
Abstract；
In mice, bone morphogenetic protein (BMP) signalling activity is known to be required for the Blimp1 (Prdm1) and Ifitm3 (mil-1/fragilis)-positive germ cell progenitor formation and for survival of primordial germ cells (PGCs), but how BMP regulates PGC development remains elusive. Here we found that Six1 and Six4 homeodomain transcription factors are the downstream to BMP signalling activity in the establishment of PGC population. Expression of Six1 in the epiblast and Six4 in PGCs were downregulated in the Bmp4 null mutant embryo. Neither Six1 null mutant nor Six4 null mutant embryos show the reduction in number of PGCs. Since Six1 and Six4 are reported to play redundant functions in several tissues, we examined Six1/Six4 double null mutant embryo and found that the double mutant embryo had reduced number of PGCs in the E13.5 embryonic gonads. On E7.5, behind the PGC formation, Dppa3/Pgc7/stella-positive PGCs are reduced in the Six1/Six4 double mutant embryo.
Preliminary studies further indicated the prospective genetic interaction between Bmp4 and Six1/Six4 in PGC formation. The Bmp4 and Six1/Six4 compound heterozygous embryo (Bmp4+/-; Six1+/-; /Six4+/-) had smaller number of PGCs than the Bmp4 heterozygous embryo (Bmp4+/-) or the Six1/Six4 heterozygous embryo (Six1+/-; /Six4+/-).
Our findings therefore highlight the cooperative function of Six1 and Six4 in the BMP signal-induced mouse germ cell formation.