Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme
Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme
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DOI：
10.1073/pnas.0913748107
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发表时间：
2010-05-18
影响因子：
11.1
通讯作者：
Nishinakamura, Ryuichi
中科院分区：
文献类型：
--
作者：
Uchiyama, Yukako;Sakaguchi, Masaji;Nishinakamura, Ryuichi
肾脏是通过后肾间质和输尿管芽这两个前体组织之间的相互作用而发育的。我们之前已经证明锌指蛋白Sall1对于输尿管芽向间质吸引至关重要。在这里，我们发现Kif26b，一个运动蛋白家族基因，是Sall1的下游靶标，该基因的破坏会导致输尿管芽吸引受损而导致肾脏发育不全。在kif26b缺失的后肾中，输尿管芽附近的间充质细胞之间的紧密粘附和整合素α 8的极化分布被破坏，导致输尿管芽引诱剂Gdnf的维持失败。体外过表达Kif26b通过与非肌球蛋白相互作用引起细胞粘附增加。因此，Kif26b对肾脏发育至关重要，因为它调节与输尿管芽接触的间充质细胞的粘附。
The kidney develops through reciprocal interactions between two precursor tissues: the metanephric mesenchyme and the ureteric bud. We previously demonstrated that the zinc finger protein Sall1 is essential for ureteric bud attraction toward the mesenchyme. Here, we show that Kif26b, a kinesin family gene, is a downstream target of Sall1 and that disruption of this gene causes kidney agenesis because of impaired ureteric bud attraction. In the Kif26b-null metanephros, compact adhesion between mesenchymal cells adjacent to the ureteric buds and the polarized distribution of integrin alpha 8 were impaired, resulting in failed maintenance of Gdnf, a critical ureteric bud attractant. Overexpression of Kif26b in vitro caused increased cell adhesion through interactions with nonmuscle myosin. Thus, Kif26b is essential for kidney development because it regulates the adhesion of mesenchymal cells in contact with ureteric buds.