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The tanning hormone, bursicon, does not act directly on the epidermis to tan the Drosophila exoskeleton.
BMC Biology ( IF 5.4 ) Pub Date : 2020-02-19 , DOI: 10.1186/s12915-020-0742-5
Justin Flaven-Pouchon 1 , Javier V Alvarez 1 , Candy Rojas 1 , John Ewer 1
Affiliation  

BACKGROUND In insects, continuous growth requires the periodic replacement of the exoskeleton. Once the remains of the exoskeleton from the previous stage have been shed during ecdysis, the new one is rapidly sclerotized (hardened) and melanized (pigmented), a process collectively known as tanning. The rapid tanning that occurs after ecdysis is critical for insect survival, as it reduces desiccation, and gives the exoskeleton the rigidity needed to support the internal organs and to provide a solid anchor for the muscles. This rapid postecdysial tanning is triggered by the "tanning hormone", bursicon. Since bursicon is released into the hemolymph, it has naturally been assumed that it would act on the epidermal cells to cause the tanning of the overlying exoskeleton. RESULTS Here we investigated the site of bursicon action in Drosophila by examining the consequences on tanning of disabling the bursicon receptor (encoded by the rickets gene) in different tissues. To our surprise, we found that rapid tanning does not require rickets function in the epidermis but requires it instead in peptidergic neurons of the ventral nervous system (VNS). Although we were unable to identify the signal that is transmitted from the VNS to the epidermis, we show that neurons that express the Drosophila insulin-like peptide ILP7, but not the ILP7 peptide itself, are involved. In addition, we found that some of the bursicon targets involved in melanization are different from those that cause sclerotization. CONCLUSIONS Our findings show that bursicon does not act directly on the epidermis to cause the tanning of the overlying exoskeleton but instead requires an intermediary messenger produced by peptidergic neurons within the central nervous system. Thus, this work has uncovered an unexpected layer of control in a process that is critical for insect survival, which will significantly alter the direction of future research aimed at understanding how rapid postecdysial tanning occurs.

中文翻译:

鞣制激素bursicon不会直接作用于表皮上晒黑果蝇外骨骼。

背景技术在昆虫中,连续生长需要定期更换外骨骼。一旦在蜕皮过程中脱落了前一阶段的外骨骼残骸,新的骨骼便迅速硬化(变硬)和变黑(色素沉着),这一过程统称为晒黑。蜕皮后发生的快速晒黑对于昆虫的生存至关重要,因为它减少了干燥,并使外骨骼具有支撑内部器官和为肌肉提供坚实锚固所需的刚度。迅速的蜕皮后鞣制是由“鞣制激素”(bursicon)触发的。由于bursicon释放到了血淋巴中,自然已经假定它会作用于表皮细胞,导致其上层外骨骼晒黑。结果在这里,我们通过检查在不同组织中禁用bursicon受体(由rick病基因编码)对晒黑的后果,调查了果蝇中bursicon的作用部位。令我们惊讶的是,我们发现快速晒黑不需要表皮的病功能,而需要腹侧神经系统(VNS)的肽能神经元需要instead病。尽管我们无法识别从VNS传输到表皮的信号,但我们显示了表达果蝇胰岛素样肽ILP7而不是ILP7肽本身的神经元。此外,我们发现,涉及黑色素化的某些bursicon目标与导致硬化的目标不同。结论我们的研究结果表明,bursicon不会直接作用于表皮上导致上覆的外骨骼晒黑,而是需要由中枢神经系统内的肽能神经元产生的中间信使。因此,这项工作发现了一个对昆虫生存至关重要的过程中不可预料的控制层,这将大大改变未来旨在了解蜕皮后快速晒黑的研究方向。
更新日期:2020-04-22
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