The transcription factor Mef2 is required for normal circadian behavior in Drosophila.
The transcription factor Mef2 is required for normal circadian behavior in Drosophila.
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DOI：
10.1523/jneurosci.2688-09.2010
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发表时间：
2010-04-28
期刊：
影响因子：
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通讯作者：
Blau J
中科院分区：
文献类型：
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作者：
Blanchard FJ;Collins B;Cyran SA;Hancock DH;Taylor MV;Blau J
转录因子Mef2在果蝇的肌肉发育和哺乳动物的许多细胞类型（包括神经元）的分化中具有公认的作用。在这里，我们描述了Mef2在调节昼夜行为节律的果蝇起搏神经元中的作用。我们发现，Mef2是正常的产生在所有的成年人的时钟神经元和Mef2过表达的时钟神经元导致长周期和复杂的节奏的成年人的运动行为。通过RNAi敲低Mef2表达或表达Mef2的阻遏物形式导致果蝇失去昼夜行为节律。这些行为变化与起搏神经元中改变的分子钟相关：Mef2过度表达导致单个起搏神经元中的振荡变得去极化，而Mef2敲低强烈抑制分子节律。因此，在时钟神经元中需要正常水平的Mef2活性来维持稳健和准确的昼夜行为节律。
The transcription factor Mef2 has well-established roles in muscle development in Drosophila and in the differentiation of many cell types in mammals, including neurons. Here, we describe a role for Mef2 in the Drosophila pacemaker neurons that regulate circadian behavioral rhythms. We found that Mef2 is normally produced in all adult clock neurons and that Mef2 over-expression in clock neurons leads to long period and complex rhythms of adult locomotor behavior. Knocking down Mef2 expression via RNAi or expressing a repressor form of Mef2 caused flies to lose circadian behavioral rhythms. These behavioral changes are correlated with altered molecular clocks in pacemaker neurons: Mef2 over-expression causes the oscillations in individual pacemaker neurons to become desynchronized, while Mef2 knockdown strongly dampens molecular rhythms. Thus, a normal level of Mef2 activity is required in clock neurons to maintain robust and accurate circadian behavioral rhythms.