A Mouse Line Expressing Sall1-Driven Inducible Cre Recombinase in the Kidney Mesenchyme
A Mouse Line Expressing Sall1-Driven Inducible Cre Recombinase in the Kidney Mesenchyme
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DOI：
10.1002/dvg.20603
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发表时间：
2010-03-01
期刊：
影响因子：
1.5
通讯作者：
Nishinakamura, Ryuichi
中科院分区：
文献类型：
--
作者：
Inoue, Shuji;Inoue, Miki;Nishinakamura, Ryuichi
Sall1在发育中的肾脏后肾间质中表达，缺乏Sall1的小鼠表现为肾脏发育不全或发育不良。Sallf也在其他部位表达，包括肢体芽、肛门、心脏和中枢神经系统。小鼠和人类中Sall1的显性阴性突变会导致这些器官的发育缺陷。在这里，我们在内源性Sall1启动子的控制下，生成了表达他莫昔芬诱导的Cre重组酶（CreER(T2)）的小鼠细胞系。经他莫昔芬治疗后，这些小鼠在内源性Sall1表达的组织中表现出基因组重组。当CreER（T2）小鼠与固定的Sall1等位基因杂交时，妊娠期服用他莫昔芬导致Sall1表达显著降低，出生时肾脏变小，表明Sall1功能被破坏。此外，新生儿他莫昔芬治疗显著降低了肾脏中Sall1的表达。Sall1CreER（T2）小鼠是体内时间依赖性和区域特异性敲除和过表达研究的宝贵工具。创世纪48:207-212,2010。(C) 2010 Wiley-Liss, Inc。
Sall1 is expressed in the metanephric mesenchyme in the developing kidney, and mice deficient in Sall1 show kidney agenesis or dysgenesis. Sallf is also expressed elsewhere, including in the limb buds, anus, heart, and central nervous system. Dominant-negative mutations of Sall1 in mice and humans lead to developmental defects in these organs. Here, we generated a mouse line expressing tamoxifen-inducible Cre recombinase (CreER(T2)) under the control of the endogenous Sall1 promoter. Upon tamoxifen treatment, these mice showed genomic recombination in the tissues where endogenous Sall1 is expressed. When CreER(T2) mice were crossed with the floxed Sall1 allele, tamoxifen administration during gestation led to a significant decrease in Sall1 expression and small kidneys at birth, suggesting that Sall1 functions were disrupted. Furthermore, Sall1 expression in the kidney was significantly reduced by neonatal tamoxifen treatment. The Sall1CreER(T2) mouse is a valuable tool for in vivo time-dependent and region-specific knockout and overexpression studies. genesis 48:207-212, 2010. (C) 2010 Wiley-Liss, Inc.