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首页> 外文期刊>Neuron >The Drosophila miR-310 cluster negatively regulates synaptic strength at the neuromuscular junction.
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The Drosophila miR-310 cluster negatively regulates synaptic strength at the neuromuscular junction.

机译:果蝇miR-310簇负调节神经肌肉接头处的突触强度。

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摘要

Emerging data implicate microRNAs (miRNAs) in the regulation of synaptic structure and function, but we know little about their role in the regulation of neurotransmission in presynaptic neurons. Here, we demonstrate that the miR-310-313 cluster is required for normal synaptic transmission at the Drosophila larval neuromuscular junction. Loss of miR-310-313 cluster leads to a significant enhancement of neurotransmitter release, which can be rescued with temporally restricted expression of mir-310-313 in larval presynaptic neurons. Kinesin family member, Khc-73 is a functional target for miR-310-313 as its expression is increased in mir-310-313 mutants and reducing it restores normal synaptic function. Cluster mutants show an increase in the active zone protein Bruchpilot accompanied by an increase in electron dense T bars. Finally, we show that repression of Khc-73 by miR-310-313 cluster influences the establishment of normal synaptic homeostasis. Our findings establish a role for miRNAs in the regulation of neurotransmitter release.
机译:新兴数据暗示了microRNA(miRNA)调控突触结构和功能,但我们对其在突触前神经元神经传递调控中的作用了解甚少。在这里,我们证明了果蝇幼虫神经肌肉连接处正常突触传递需要miR-310-313簇。 miR-310-313簇的丢失导致神经递质释放的显着增强,可以通过在幼虫突触前神经元中暂时限制mir-310-313的表达来挽救神经递质的释放。 Kinesin家族成员Khc-73是miR-310-313的功能靶标,因为它在mir-310-313突变体中的表达增加,而其表达降低则恢复了正常的突触功能。簇状突变体显示出活性区蛋白Bruchpilot的增加,伴随着电子致密T条的增加。最后,我们证明了miR-310-313簇抑制Khc-73会影响正常突触稳态的建立。我们的发现确定了miRNA在调节神经递质释放中的作用。

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