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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Conserved Role For The Drosophila Pax6 Homolog Eyeless In Differentiation And Function Of Insulin-producing Neurons
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Conserved Role For The Drosophila Pax6 Homolog Eyeless In Differentiation And Function Of Insulin-producing Neurons

机译：果蝇Pax6同源物在产生胰岛素的神经元的分化和功能中无眼的保守作用

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摘要

Insulin/insulin-like growth factor (IGF) signaling constitutes an evolutionary conserved pathway that controls growth, energy homeostasis, and longevity. In Drosophila melanogaster, key components of this pathway are the insulin-like peptides (Dilps). The major source of Dilps is a cluster of large neurons in the brain, the insulin-producing cells (IPCs). The genetic control of IPC development and function is poorly understood. Here, we demonstrate that the Pax6 homolog Eyeless is required in the IPCs to control their differentiation and function. Loss of eyeless results in phe-notypes associated with loss of insulin signaling, including decreased animal size and increased carbohydrate levels in larval hemolymph. We show that mutations in eyeless lead to defective differentiation and morphologically abnormal IPCs. We also demonstrate that Eyeless controls IPC function by the direct transcrip-tional control of one of the major Dilps, dilpS. We propose that Eyeless has an evolutionarily conserved role in IPCs with remarkable similarities to the role of vertebrate Pax6 in β cells of the pancreas.
机译：胰岛素/胰岛素样生长因子（IGF）信号传导构成控制生长，能量稳态和寿命的进化保守途径。在果蝇中，该途径的关键成分是胰岛素样肽（Dilps）。 Dilps的主要来源是大脑中的大型神经元簇，即胰岛素产生细胞（IPC）。对IPC发育和功能的遗传控制了解甚少。在这里，我们证明了IPC需要Pax6同系物Eyeless来控制其分化和功能。失去视力会导致与胰岛素信号传导丧失相关的表型，包括动物体型减小和幼虫血淋巴中碳水化合物含量增加。我们表明，无眼中的突变导致缺陷的分化和形态异常的IPC。我们还证明了Eyeless通过主要Dilps之一dilpS的直接转录控制来控制IPC功能。我们提出，Eyeless在IPC中具有进化保守的作用，与脊椎动物Pax6在胰腺β细胞中的作用具有显着相似性。

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