論文

査読有り
2010年3月

Overexpression of Sall1 in vivo leads to reduced body weight without affecting kidney development

JOURNAL OF BIOCHEMISTRY
  • Qing Jiang
  • ,
  • Sayoko Fujimura
  • ,
  • Chiyoko Kobayashi
  • ,
  • Ryuichi Nishinakamura

147
3
開始ページ
445
終了ページ
450
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1093/jb/mvp214
出版者・発行元
OXFORD UNIV PRESS

Human SALL1 is a homologue of the Drosophila region-specific homeotic gene sal, and is also known as a causative gene for Townes-Brocks syndrome, which is characterized by multi-organ malformations. We previously demonstrated that mouse Sall1 plays a crucial role in ureteric bud invasion during kidney development, and possibly in nephron progenitor cells in the metanephric mesenchyme. To gain insights into the Sall1 functions in the kidney and other tissues, we generated R26Sall1 mice, in which Rosa26 locus stop sequences flanked by two loxP sites were located upstream of the Sall1 cDNA. This allele allowed exogenous Sall1 expression in a Cre recombinase-dependent manner. R26Sall1 mice were first crossed with CAGCre mice, which expressed Cre recombinase ubiquitously during embryogenesis. Mice expressing Sall1 ubiquitously were smaller in size compared with mice of other genotypes. We then crossed R26Sall1 mice with Six2Cre mice expressing Cre recombinase in the metanephric mesenchyme during kidney development. However, no kidney defects were observed. Taken together, overexpression of Sall1 does not affect kidney development, but does lead to a reduced body weight, suggesting that the optimal dosage of Sall1 is required for normal mouse development.

Web of Science ® 被引用回数 : 3

リンク情報
DOI
https://doi.org/10.1093/jb/mvp214
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000274777300016&DestApp=WOS_CPL