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首页> 外文期刊>Neuron >Hsc70-4 Deforms Membranes to Promote Synaptic Protein Turnover by Endosomal Microautophagy
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Hsc70-4 Deforms Membranes to Promote Synaptic Protein Turnover by Endosomal Microautophagy

机译：Hsc70-4变形膜，通过内体微自噬促进突触蛋白的转换。

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Synapses are often far from their cell bodies and must largely independently cope with dysfunctional proteins resulting from synaptic activity and stress. To identify membrane-associated machines that can engulf synaptic targets destined for degradation, we performed a large-scale in vitro liposome-based screen followed by functional studies. We identified a presynaptically enriched chaperone Hsc70-4 that bends membranes based on its ability to oligomerize. This activity promotes endosomal microautophagy and the turnover of specific synaptic proteins. Loss of microautophagy slows down neurotransmission while gain of microautophagy increases neurotransmission. Interestingly, Sgt, a cochaperone of Hsc70-4, is able to switch the activity of Hsc70-4 from synaptic endosomal microautophagy toward chaperone activity. Hence, Hsc70-4 controls rejuvenation of the synaptic protein pool in a dual way: either by refolding proteins together with Sgt, or by targeting them for degradation by facilitating endosomal microautophagy based on its membrane deforming activity.
机译：突触通常远离它们的细胞体，并且必须在很大程度上独立地应对由突触活性和压力导致的功能异常的蛋白质。为了确定可以吞噬拟降解的突触靶标的膜相关机器，我们进行了大规模的体外脂质体筛选，随后进行了功能研究。我们发现了一个突触前丰富的伴侣Hsc70-4，它基于寡聚的能力使膜弯曲。该活性促进内体微自噬和特定突触蛋白的更新。微自噬的丧失会减慢神经传递，而微自噬的获得会增加神经传递。有趣的是，Sgt，Hsc70-4的伴侣分子，能够将Hsc70-4的活性从突触内体微自噬转变为伴侣活性。因此，Hsc70-4以双重方式控制突触蛋白库的恢复：通过将蛋白与Sgt一起重新折叠，或通过基于其膜变形活性促进内体微自噬而将其靶向降解。

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