DPP-mediated TGFβ signaling regulates juvenile hormone biosynthesis by activating the expression of juvenile hormone acid methyltransferase
DPP-mediated TGFβ signaling regulates juvenile hormone biosynthesis by activating the expression of juvenile hormone acid methyltransferase
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DOI：
10.1242/dev.057687
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发表时间：
2011-06-01
期刊：
影响因子：
4.6
通讯作者：
Wang, Jian
中科院分区：
文献类型：
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作者：
Huang, Jianhua;Tian, Ling;Wang, Jian
扁桃体(CA)中保幼激素(JH)的生物合成受大脑产生的神经肽和神经递质的调节。然而，关于这些神经信号如何导致JH生物合成的变化，人们知之甚少。在这里，我们报告了一种新的功能，即转化生长因子β信号将脑信号转化为JH酸甲基转移酶(JHAMT)的转录变化，JHAMT是JH生物合成的关键调节酶。果蝇的遗传筛选表明，Tkv和Mad是JH介导的抑制幼虫br广泛表达所必需的。进一步的研究表明，转化生长因子β信号通过上调Jhamt的表达来刺激JH的生物合成。此外，DPP亚型突变还诱导性早熟br的表达。外源JH激动剂部分挽救了这些DPP突变体的幼虫致死性。最后，DPP在环腺的CA细胞中特异表达，其在CA中的表达谱与JHAMT的表达谱相关，并与血淋巴中JH的表达水平相匹配。在Nmdar1的突变幼虫中检测到DPP表达减少，Nmdar1是CA表达的谷氨酸受体。综上所述，我们得出结论，神经递质谷氨酸促进了CA中DPP的表达，DPP通过Tkv和Mad通过上调Jhamt在幼虫早期阶段的转录来刺激JH的生物合成，以防止早熟变态。
Juvenile hormone (JH) biosynthesis in the corpus allatum (CA) is regulated by neuropeptides and neurotransmitters produced in the brain. However, little is known about how these neural signals induce changes in JH biosynthesis. Here, we report a novel function of TGF beta signaling in transferring brain signals into transcriptional changes of JH acid methyltransferase (jhamt), a key regulatory enzyme of JH biosynthesis. A Drosophila genetic screen identified that Tkv and Mad are required for JH-mediated suppression of broad (br) expression in young larvae. Further investigation demonstrated that TGF beta signaling stimulates JH biosynthesis by upregulating jhamt expression. Moreover, dpp hypomorphic mutants also induced precocious br expression. The pupal lethality of these dpp mutants was partially rescued by an exogenous JH agonist. Finally, dpp was specifically expressed in the CA cells of ring glands, and its expression profile in the CA correlated with that of jhamt and matched JH levels in the hemolymph. Reduced dpp expression was detected in larvae mutant for Nmdar1, a CA-expressed glutamate receptor. Taken together, we conclude that the neurotransmitter glutamate promotes dpp expression in the CA, which stimulates JH biosynthesis through Tkv and Mad by upregulating jhamt transcription at the early larval stages to prevent premature metamorphosis.