Xu Jingxia, Krebs Luke T, Gridley Thomas
The Jackson Laboratory, Bar Harbor, Maine 04609, USA.
Genesis. 2010 Jun;48(6):390-3. doi: 10.1002/dvg.20626.
The Notch signaling pathway is an evolutionarily-conserved intercellular signaling mechanism, and mutations in its components disrupt embryonic development in many organisms and cause inherited diseases in humans. The Jagged2 (Jag2) gene, which encodes a ligand for Notch pathway receptors, is required for craniofacial, limb, and T cell development. Mice homozygous for a Jag2 null allele die at birth from cleft palate, precluding study of Jag2 function in postnatal and adult mice. We have generated a Jag2 conditional null allele by flanking the first two exons of the Jag2 gene with loxP sites. Cre-mediated deletion of the Jag2(flox) allele generates the Jag2(del2) allele, which behaves genetically as a Jag2 null allele. This Jag2 conditional null allele will enable investigation of Jag2 function in a variety of tissue-specific contexts.
Notch信号通路是一种在进化上保守的细胞间信号传导机制,其组成成分的突变会破坏许多生物体的胚胎发育,并导致人类遗传性疾病。锯齿状蛋白2(Jag2)基因编码Notch信号通路受体的配体,对颅面、肢体和T细胞发育至关重要。Jag2无效等位基因的纯合小鼠出生时因腭裂死亡,这使得无法研究Jag2在出生后和成年小鼠中的功能。我们通过在Jag2基因的前两个外显子两侧插入loxP位点,生成了一个Jag2条件性无效等位基因。Cre介导的Jag2(flox)等位基因缺失产生Jag2(del2)等位基因,其在遗传行为上表现为Jag2无效等位基因。这种Jag2条件性无效等位基因将有助于在多种组织特异性背景下研究Jag2的功能。