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脂肪细胞因子 NimrodB5 调控果蝇外周造血。

The adipokine NimrodB5 regulates peripheral hematopoiesis in Drosophila.

机构信息

Global Health Institute, School of Life Science, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.

Centre de Génétique Moléculaire CNRS, Université Pierre et Marie Curie, Gif-sur-Yvette, France.

出版信息

FEBS J. 2020 Aug;287(16):3399-3426. doi: 10.1111/febs.15237. Epub 2020 Feb 17.

DOI:10.1111/febs.15237
PMID:32009293
Abstract

In animals, growth is regulated by the complex interplay between paracrine and endocrine signals. When food is scarce, tissues compete for nutrients, leading to critical resource allocation and prioritization. Little is known about how the immune system maturation is coordinated with the growth of other tissues. Here, we describe a signaling mechanism that regulates the number of hemocytes (blood cells) according to the nutritional state of the Drosophila larva. Specifically, we found that a secreted protein, NimB5, is produced in the fat body upon nutrient scarcity downstream of metabolic sensors and ecdysone signaling. NimB5 is then secreted and binds to hemocytes to down-regulate their proliferation and adhesion. Blocking this signaling loop results in conditional lethality when larvae are raised on a poor diet, due to excessive hemocyte numbers and insufficient energy storage. Similar regulatory mechanisms shaping the immune system in response to nutrient availability are likely to be widespread in animals.

摘要

在动物中,生长受到旁分泌和内分泌信号之间复杂相互作用的调节。当食物匮乏时,组织会争夺营养物质,导致关键资源的分配和优先化。关于免疫系统的成熟如何与其他组织的生长相协调,人们知之甚少。在这里,我们描述了一种信号机制,该机制根据果蝇幼虫的营养状态来调节血细胞(血细胞)的数量。具体来说,我们发现一种分泌蛋白 NimB5 在营养匮乏时由代谢传感器和蜕皮激素信号下游的脂肪体产生。然后,NimB5 被分泌并与血细胞结合,以下调其增殖和黏附。当幼虫在不良饮食中生长时,阻断这条信号通路会导致条件性致死,这是由于血细胞数量过多和能量储存不足所致。类似的调节机制可能在动物中广泛存在,以响应营养物质的可用性来塑造免疫系统。

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