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首页> 外文期刊>The European Journal of Neuroscience >Myocyte enhancer factor-2 and p300 interact to regulate the expression of homeostatic regulator Pumilio in Drosophila
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Myocyte enhancer factor-2 and p300 interact to regulate the expression of homeostatic regulator Pumilio in Drosophila

机译：肌细胞增强剂因子-2和P300相互作用以调节傲慢性调节器Pumilio在果蝇中的表达

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摘要

Pumilio (Pum), an RNA-binding protein, is a key component of neuron firing-rate homeostasis that likely maintains stability of neural circuit activity in all animals, from flies to mammals. While Pum is ubiquitously expressed, we understand little about how synaptic excitation regulates its expression in the CNS. Here, we characterized the Drosophila dpum promoter and identified multiple myocyte enhancer factor-2 (Mef2)-binding elements. We cloned 12 dmef2 splice variants and used a luciferase-based assay to monitor dpum promoter activity. While all 12 dMef2 splice variants enhance dpum promoter activity, exon 10-containing variants induce greater transactivation. Previous work shows dPum expression increases with synaptic excitation. However, we observe no change in dmef2 transcript in larval CNS, of both sexes, exposed to the proconvulsant picrotoxin. The lack of activity dependence is indicative of additional regulation. We identified p300 as a potential candidate. We show that by binding to dMef2, p300 represses dpum transactivation. Significantly, p300 transcript is downregulated by enhanced synaptic excitation (picrotoxin) which, in turn, increases transcription of dpum through derepression of dMef2. These results advance our understanding of dpum by showing the activity-dependent expression is regulated by an interaction between p300 and dMef2.
机译：Pumilio（Pum）是RNA结合蛋白，是神经元烧制率稳态的关键组分，其可能在苍蝇到哺乳动物中保持所有动物中神经电路活性的稳定性。虽然普遍表达了PUM，但我们很少了解突触激发如何调节其在CNS中的表达。在这里，我们表征了果蝇DPUM启动子，并鉴定了多种肌细胞增强子因子-2（MEF2） - 耦合元素。我们克隆了12 DMEF2剪接变体并使用了基于荧光素酶的测定来监测DPUM启动子活性。虽然所有12dmef2剪接变体增强DPUM启动子活性，但外显子10的变体诱导更大的转移激活。以前的工作显示DPUM表达随突触激发增加。然而，我们观察到两性的幼虫CNS中的DMEF2转录物的变化，暴露于ProconVulstant Picrotoxin。缺乏活动依赖性表明额外的规定。我们将P300确定为潜在的候选人。我们表明，通过与DMEF2结合，P300抑制DPUM转移激活。显着地，P300转录物通过增强的突触激发（微毒素）来下调，其又增加DPUM的转录通过DMEF2。这些结果通过显示活动依赖性表达通过P300和DMEF2之间的相互作用来调节对DPUM的理解。

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