アクティブボード・２０１３年　１月
　　　　　・・・・・２０１３年　１月　４日更新・・・・・

研究発表を行った学会；
・第３５回日本分子生物学会年会
　２０１２年１２月１１日〜１４日（福岡）

タイトル；The role of Sall1 in the kidney development.

発表者；神田　祥一郎　氏
　　　（熊本大学　発生医学研究所　腎臓発生分野）
Abstract；
The kidney develops through the reciprocal interaction between the ureteric bud (UB) and the metanephric mesenchyme (MM). The MM surrounding the UB, called the cap mesenchyme (CM), is characterized by the elevated expression of Six2. The CM represents the nephron progenitors.
In the mouse embryonic kidney, both the CM and the differentiating nephrons express the transcriptional factor Sall1. While Sall1 plays an important role in the kidney development, the precise mechanism has not been clarified. Here we investigated the molecular mechanisms of Sall1 in the kidney development.
To examine the requirement for Sall1 in the CM, we generated Sall1 floxed mice and intercrossed these mice to Six2-Cre mice. The mutant kidneys were reduced in size and showed poor maintenance of nephron progenitors. We next generated a Sall1-Flag knock-in mouse line and found that Sall1 was bound to HDAC2 and Mi2β. Then we performed microarray analysis and in situ hybridization, which showed that an up-regulated gene in the Sall1-null mice was expressed in the differentiating nephrons.
These results indicate that Sall1 could suppress aberrant gene expression in the differentiating nephrons.