Podosome-regulating kinesin KIF1C translocates to the cell periphery in a CLASP-dependent manner
Podosome-regulating kinesin KIF1C translocates to the cell periphery in a CLASP-dependent manner
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DOI：
10.1242/jcs.149633
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发表时间：
2014-12-15
影响因子：
4
通讯作者：
Kaverina, Irina
中科院分区：
文献类型：
--
作者：
Efimova, Nadia;Grimaldi, Ashley;Kaverina, Irina
众所周知，驱动蛋白 KIF1C 可以调节足小体，即富含肌动蛋白的粘附结构，在生理过程中重塑细胞外基质。在这里，我们证明 KIF1C 是足体诱导信号级联中的一个参与者。在蛋白激酶 C (PKC) 诱导足小体形成后，KIF1C 易位到细胞周围的情况加剧，并且 KIF1C 在外周微管附近积聚，显示出加尖相关蛋白 CLASP 和足小体周围的富集。重要的是，如果没有 CLASP，KIF1C 的运输和足小体的形成都会受到抑制。此外，嵌合线粒体靶向 CLASP2 招募 KIF1C，表明存在短暂的 CLASP-KIF1C 关联。我们建议 CLASP 为 KIF1C 创建首选微管轨道，以促进 PKC 下游足体诱导。
The kinesin KIF1C is known to regulate podosomes, actin-rich adhesion structures that remodel the extracellular matrix during physiological processes. Here, we show that KIF1C is a player in the podosome-inducing signaling cascade. Upon induction of podosome formation by protein kinase C (PKC), KIF1C translocation to the cell periphery intensifies and KIF1C accumulates both in the proximity of peripheral microtubules that show enrichment for the plus-tip-associated proteins CLASPs and around podosomes. Importantly, without CLASPs, both KIF1C trafficking and podosome formation are suppressed. Moreover, chimeric mitochondrially targeted CLASP2 recruits KIF1C, suggesting a transient CLASP-KIF1C association. We propose that CLASPs create preferred microtubule tracks for KIF1C to promote podosome induction downstream of PKC.