Desmosomal cadherins utilize distinct kinesins for assembly into desmosomes.
Desmosomal cadherins utilize distinct kinesins for assembly into desmosomes.
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DOI：
10.1083/jcb.201106057
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发表时间：
2011-12-26
期刊：
影响因子：
--
通讯作者：
Green KJ
中科院分区：
文献类型：
--
作者：
Nekrasova OE;Amargo EV;Smith WO;Chen J;Kreitzer GE;Green KJ
桥粒芯糖蛋白和桥粒芯胶蛋白通过不同的驱动蛋白马达转运到质膜，提供了在发育和上皮重塑期间定制桥粒结构和功能的潜在机制。桥粒钙粘蛋白，桥粒糖蛋白（Dsgs）和桥粒柯林斯（Dscs），构成细胞间连接的粘附核心，称为桥粒。尽管已知这些粘附分子对组织完整性至关重要，但协调它们进入细胞间连接以调节其适当比例和分布的机制尚不清楚。我们证明，Dsg 2和Dsc 2都表现出微管依赖性运输上皮细胞，但使用不同的电机交通质膜。与驱动蛋白-1阻断Dsg 2运输的功能干扰，导致Dsg 2缺陷的接头的组装，对Dsc 2或桥粒斑块组分的分布影响最小。相反，抑制驱动蛋白-2阻止Dsc 2运动，并减少其质膜积累，而不影响Dsg 2的运输。无论是驱动蛋白-1或-2缺乏削弱细胞间粘附，尽管在质膜上的粘附连接和其他桥粒成分的维护。桥粒钙粘蛋白转运的差异调节可以提供在组织形态发生和重塑过程中定制粘附强度的机制。
Desmogleins and desmocollins are transported to the plasma membrane by different kinesin motors, providing a potential mechanism to tailor desmosome structure and function during development and epithelial remodeling. The desmosomal cadherins, desmogleins (Dsgs) and desmocollins (Dscs), comprise the adhesive core of intercellular junctions known as desmosomes. Although these adhesion molecules are known to be critical for tissue integrity, mechanisms that coordinate their trafficking into intercellular junctions to regulate their proper ratio and distribution are unknown. We demonstrate that Dsg2 and Dsc2 both exhibit microtubule-dependent transport in epithelial cells but use distinct motors to traffic to the plasma membrane. Functional interference with kinesin-1 blocked Dsg2 transport, resulting in the assembly of Dsg2-deficient junctions with minimal impact on distribution of Dsc2 or desmosomal plaque components. In contrast, inhibiting kinesin-2 prevented Dsc2 movement and decreased its plasma membrane accumulation without affecting Dsg2 trafficking. Either kinesin-1 or -2 deficiency weakened intercellular adhesion, despite the maintenance of adherens junctions and other desmosome components at the plasma membrane. Differential regulation of desmosomal cadherin transport could provide a mechanism to tailor adhesion strength during tissue morphogenesis and remodeling.
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影响因子：
7.8
作者：
HIROKAWA, N;SATOYOSHITAKE, R;BRADY, ST
通讯作者：
BRADY, ST
影响因子：
56.9
作者：
Brummelkamp, TR;Bernards, R;Agami, R
通讯作者：
Agami, R
影响因子：
64.8
作者：
COLE, DG;CHINN, SW;SCHOLEY, JM
通讯作者：
SCHOLEY, JM
DOI：
10.1083/jcb.138.1.193
发表时间：
1997-07-14
期刊：
The Journal of cell biology
影响因子：
--
作者：
Chitaev NA;Troyanovsky SM
通讯作者：
Troyanovsky SM
影响因子：
3.3
作者：
Cole, NB;Sciaky, N;LippincottSchwartz, J
通讯作者：
LippincottSchwartz, J