Functional dissection of a neuronal network required for cuticle tanning and wing expansion in Drosophila
Functional dissection of a neuronal network required for cuticle tanning and wing expansion in Drosophila
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DOI：
10.1523/jneurosci.3916-05.2006
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发表时间：
2006-01-11
影响因子：
5.3
通讯作者：
White, BH
中科院分区：
文献类型：
--
作者：
Luan, HJ;Lemon, WC;White, BH
此前已有研究表明，表达甲壳动物心脏活性多肽(CCAP)的果蝇神经元亚群可以产生法氏囊激素，这是羽化后角质层晒黑和翅膀扩张所必需的。在这里，我们提出的证据表明，表达CCAP的神经元(N-CCAP)由两个不同的功能群组成，一个向血淋巴释放法氏囊素，另一个调节其释放。第一组，我们称之为N-CCAP-C929，包括14个腹神经节表达滑囊素的神经元，它们位于增强子陷阱系C929-Gal4的表达模式中。我们发现，抑制这一组中的活性会阻止法氏囊释放到血淋巴中，并伴随着晒黑和翅膀扩张。第二组，我们称之为N-CCAP-R，由C929-Gal4模式外的N-CCAP神经元组成。由于在整个N-CCAP中抑制突触传递和蛋白激酶A(PKA)的活性，但在N-CCAP-C929中不抑制，也阻止了晒黑和翅膀的扩张，因此我们得出结论，N-CCAP-R需要神经传递和PKA来调节N-CCAP-C929的滑囊素分泌。细菌钠通道NaChBac的表达增强了N-CCAP-R的电活动，也阻止了晒黑和翅膀的扩张，并导致中央过程中的法氏囊的耗尽。NaChBac在N-CCAP-C929中的表达没有影响，这表明腹部分泌法氏囊的神经元可能是沉默的，直到被刺激释放激素。我们的结果表明，N-CCAP形成了一个负责调节和释放滑囊素的相互作用的神经元网络，并提出了一个模型，在该模型中，PKA介导刺激正常静止的滑囊素表达神经元的输入，激活了激素的释放。
A subset of Drosophila neurons that expresses crustacean cardioactive peptide (CCAP) has been shown previously to make the hormone bursicon, which is required for cuticle tanning and wing expansion after eclosion. Here we present evidence that CCAP-expressing neurons (N-CCAP) consist of two functionally distinct groups, one of which releases bursicon into the hemolymph and the other of which regulates its release. The first group, which we call N-CCAP-c929, includes 14 bursicon-expressing neurons of the abdominal ganglion that lie within the expression pattern of the enhancer-trap line c929-Gal4. We show that suppression of activity within this group blocks bursicon release into the hemolymph together with tanning and wing expansion. The second group, which we call N-CCAP-R, consists of N-CCAP neurons outside the c929-Gal4 pattern. Because suppression of synaptic transmission and protein kinase A (PKA) activity throughout N-CCAP, but not in N-CCAP-c929, also blocks tanning and wing expansion, we conclude that neurotransmission and PKA are required in N-CCAP-R to regulate bursicon secretion from N-CCAP-c929. Enhancement of electrical activity in N-CCAP-R by expression of the bacterial sodium channel NaChBac also blocks tanning and wing expansion and leads to depletion of bursicon from central processes. NaChBac expression in N-CCAP-c929 is without effect, suggesting that the abdominal bursicon-secreting neurons are likely to be silent until stimulated to release the hormone. Our results suggest that N-CCAP form an interacting neuronal network responsible for the regulation and release of bursicon and suggest a model in which PKA-mediated stimulation of inputs to normally quiescent bursicon-expressing neurons activates release of the hormone.