Meng Wenxiang, Mushika Yoshimi, Ichii Tetsuo, Takeichi Masatoshi
RIKEN Center for Developmental Biology, Chuo-ku, Kobe 650-0047, Japan.
Cell. 2008 Nov 28;135(5):948-59. doi: 10.1016/j.cell.2008.09.040.
Epithelial cells contain noncentrosomal microtubules (MTs), whose minus ends are oriented apically. In contrast with the well-known interactions of the minus ends with the centrosome, little is known about the termination site of the noncentrosomal minus ends. Here we show that a population of MT minus ends is anchored at the zonula adherens (ZA), the apical-most part of the cadherin-based adherens junction, via a protein that we have termed Nezha. We initially identified PLEKHA7 as a ZA component and subsequently detected Nezha as a partner for PLEKHA7. Nezha bound MTs at their minus ends and tethered them to the ZA. Furthermore, we found that a minus end-directed motor, KIFC3, was concentrated at the ZA in a PLEKHA7/Nezha/MT-dependent manner; and depletion of any of these proteins resulted in disorganization of the ZA. We propose that the PLEKHA7/Nezha/MT complex regulates the ZA integrity by recruiting KIFC3 to this junctional site.
上皮细胞含有非中心体微管(MTs),其负端朝向顶端。与负端与中心体的众所周知的相互作用不同,关于非中心体负端的终止位点知之甚少。在这里,我们表明,一群MT负端通过一种我们称为哪吒的蛋白质锚定在黏着小带(ZA),即基于钙黏蛋白的黏附连接的最顶端部分。我们最初将PLEKHA7鉴定为ZA成分,随后检测到哪吒是PLEKHA7的伙伴。哪吒在MT的负端结合MT,并将它们拴系到ZA。此外,我们发现一种负端定向马达KIFC3以PLEKHA7/哪吒/MT依赖的方式集中在ZA;这些蛋白质中的任何一种缺失都会导致ZA的紊乱。我们提出,PLEKHA7/哪吒/MT复合物通过将KIFC3招募到这个连接位点来调节ZA的完整性。