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Unique characteristics of Ca~(2+) homeostasis of the trans-Golgi compartment

机译:反式高尔基体Ca〜(2+)稳态的独特特征

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Taking advantage of a fluorescent Ca~(2+) indicator selectively targeted to the trans-Golgi lumen, we here demonstrate that its Ca~(2+) homeostatic mechanisms are distinct from those of the other Golgi subcompartments: (ⅰ) Ca~(2+) uptake depends exclusively on the activity of the secretory pathway Ca~(2+) ATPasei (SPCA1), whereas the sarco-endoplasmic reticulum Ca~(2+) ATPase (SERCA) is excluded; (ⅱ) IP_3 generated by receptor stimulation causes Ca~(2+) uptake rather than release; (ⅲ) Ca~(2+) release can be triggered by activation of rya-nodine receptors in cells endowed with robust expression of the latter channels (e.g., in neonatal cardiac myocyte). Finally, we show that, knocking down the SPCA1, and thus altering the trans-Golgi Ca~(2+) content, specific functions associated with this subcompart-ment, such as sorting of proteins to the plasma membrane through the secretory pathway, and the structure of the entire Golgi apparatus are dramatically altered.
机译:利用选择性靶向反式高尔基体腔的荧光Ca〜(2+)指示剂,我们在这里证明了其Ca〜(2+)稳态机制不同于其他高尔基子区隔:(ⅰ)Ca〜( 2+)的摄取仅取决于分泌途径Ca〜(2+)ATPasei(SPCA1)的活性,而肌内质网Ca〜(2+)ATPase(SERCA)除外; (ⅱ)受体刺激产生的IP_3引起Ca〜(2+)的吸收而不是释放; (ⅲ)Ca〜(2+)的释放可以通过激活具有后一通道强力表达的细胞(例如,在新生儿心肌细胞中)中的rya-nodine受体来激活。最后,我们表明,敲低SPCA1,从而改变反式高尔基Ca〜(2+)的含量,与该小室相关的特定功能,例如通过分泌途径将蛋白分类到质膜,以及整个高尔基体的结构发生了巨大变化。

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