An epidermal plakin that integrates actin and microtubule networks at cellular junctions.
An epidermal plakin that integrates actin and microtubule networks at cellular junctions.
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DOI：
10.1083/jcb.149.1.195
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发表时间：
2000-04-03
期刊：
影响因子：
--
通讯作者：
Fuchs E
中科院分区：
文献类型：
--
作者：
Karakesisoglou I;Yang Y;Fuchs E
Plakins是细胞骨架连接蛋白，最初被认为只与中间丝（IF）相互作用，但最近发现还与肌动蛋白和微管网络相关。在这里，我们报告的ACF 7，哺乳动物直系同源的果蝇鸮鹦鹉斑基因参与表皮肌肉粘连和神经肌肉接头。虽然ACF 7/kakapo在其IF结合结构域上与其他斑因子不同，但它至少有一个肌动蛋白（Kd = 0.35 μM）和一个微管（Kd = 6 μM）结合结构域。与果蝇类似，ACF 7在表皮中表达。在分布良好的表皮角质形成细胞中，ACF 7不连续地装饰细胞周边的细胞骨架，包括在焦点接触处平行排列会聚的微管（MT）和肌动蛋白丝（AF）。在钙诱导细胞间粘附后，ACF 7和细胞骨架在细胞-细胞边界重组，但具有与粘附连接和桥粒不同的动力学。用细胞骨架解聚药物的治疗揭示了ACF 7的细胞骨架缔合依赖于微管网络，但ACF 7似乎也在微管和微丝相遇的位点稳定肌动蛋白。我们认为ACF 7可能在微管动力学中起作用，以促进肌动蛋白-微管在细胞外周的相互作用，并将微管网络耦合到细胞连接处。这些属性提供了一个明确的解释鸮鹦鹉突变型的苍蝇。
Plakins are cytoskeletal linker proteins initially thought to interact exclusively with intermediate filaments (IFs), but recently were found to associate additionally with actin and microtubule networks. Here, we report on ACF7, a mammalian orthologue of the Drosophila kakapo plakin genetically involved in epidermal–muscle adhesion and neuromuscular junctions. While ACF7/kakapo is divergent from other plakins in its IF-binding domain, it has at least one actin (K d = 0.35 μM) and one microtubule (K d ∼6 μM) binding domain. Similar to its fly counterpart, ACF7 is expressed in the epidermis. In well spread epidermal keratinocytes, ACF7 discontinuously decorates the cytoskeleton at the cell periphery, including microtubules (MTs) and actin filaments (AFs) that are aligned in parallel converging at focal contacts. Upon calcium induction of intercellular adhesion, ACF7 and the cytoskeleton reorganize at cell–cell borders but with different kinetics from adherens junctions and desmosomes. Treatments with cytoskeletal depolymerizing drugs reveal that ACF7's cytoskeletal association is dependent upon the microtubule network, but ACF7 also appears to stabilize actin at sites where microtubules and microfilaments meet. We posit that ACF7 may function in microtubule dynamics to facilitate actin–microtubule interactions at the cell periphery and to couple the microtubule network to cellular junctions. These attributes provide a clear explanation for the kakapo mutant phenotype in flies.
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