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首页> 外文期刊>Neuron >Regulation of dendritogenesis via a lipid-raft-associated Ca2+/calmodulin-dependent protein kinase CLICK-III/CaMKIgamma.
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Regulation of dendritogenesis via a lipid-raft-associated Ca2+/calmodulin-dependent protein kinase CLICK-III/CaMKIgamma.

机译：通过脂筏相关的Ca2 + /钙调蛋白依赖性蛋白激酶CLICK-III / CaMKIgamma调节树突形成。

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摘要

Ca(2+) signaling plays a central role in activity-dependent regulation of dendritic arborization, but key molecular mechanisms downstream of calcium elevation remain poorly understood. Here we show that the C-terminal region of the Ca(2+)/calmodulin-dependent protein kinase CLICK-III (CL3)/CaMKIgamma, a membrane-anchored CaMK, was uniquely modified by two sequential lipidification steps: prenylation followed by a kinase-activity-regulated palmitoylation. These modifications were essential for CL3 membrane anchoring and targeting into detergent-resistant lipid microdomains (or rafts) in the dendrites. We found that CL3 critically contributed to BDNF-stimulated dendritic growth. Raft insertion of CL3 specifically promoted dendritogenesis of cortical neurons by acting upstream of RacGEF STEF and Rac, both present in lipid rafts. Thus, CL3 may represent a key element in the Ca(2+)-dependent and lipid-raft-delineated switch that turns on extrinsic activity-regulated dendrite formation in developing corticalneurons.
机译：Ca（2+）信号在树突状乔木的活性依赖调节中发挥中心作用，但钙升高下游的关键分子机制仍然知之甚少。在这里，我们显示Ca（2 +）/钙调蛋白依赖性蛋白激酶CLICK-III（CL3）/ CaMKIgamma（膜锚定的CaMK）的C端区域通过两个连续的脂化步骤被独特地修饰：异戊烯化然后加激酶活性调节的棕榈酰化。这些修饰对于CL3膜锚定并靶向树突中耐去污剂的脂质微区（或筏）至关重要。我们发现CL3关键促成BDNF刺激的树突状生长。通过在脂筏中存在的RacGEF STEF和Rac的上游起作用，CL3的筏插入可以特异性地促进皮质神经元的树突形成。因此，CL3可能代表在Ca（2+）依赖和脂质筏描绘的开关中的关键元素，该开关打开外在活性调节发育中的皮层神经元的枝晶形成。

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