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成虫盘生长因子2和3参与果蝇对线虫感染的反应。

The Imaginal Disc Growth Factors 2 and 3 participate in the Drosophila response to nematode infection.

作者信息

Yadav Shruti, Eleftherianos Ioannis

机构信息

Department of Biological Sciences, The George Washington University, Washington, District of Columbia.

出版信息

Parasite Immunol. 2018 Oct;40(10):e12581. doi: 10.1111/pim.12581. Epub 2018 Sep 14.

Abstract

The Drosophila imaginal disc growth factors (IDGFs) induce the proliferation of imaginal disc cells and terminate cell proliferation at the end of larval development. However, the participation of Idgf-encoding genes in other physiological processes of Drosophila including the immune response to infection is not fully understood. Here, we show the contribution of Idgf2 and Idgf3 in the Drosophila response to infection with Steinernema carpocapsae nematodes carrying or lacking their mutualistic Xenorhabdus nematophila bacteria (symbiotic or axenic nematodes, respectively). We find that Idgf2 and Idgf3 are upregulated in Drosophila larvae infected with symbiotic or axenic Steinernema and inactivation of Idgf2 confers a survival advantage to Drosophila larvae against axenic nematodes. Inactivation of Idgf2 induces the Imd and Jak/Stat pathways, whereas inactivation of Idgf3 induces the Imd, Toll and Jak/Stat pathways. We also show that inactivation of the Imd pathway receptor PGRP-LE upregulates Idgf2 against Steinernema nematode infection. Finally, we demonstrate that inactivation of Idgf3 induces the recruitment of larval haemocytes in response to Steinernema. Our results indicate that Idgf2 and Idgf3 might be involved in different yet crucial immune functions in the Drosophila antinematode immune response. Similar findings will promote the development of new targets for species-specific pest control strategies.

摘要

果蝇成虫盘生长因子(IDGFs)可诱导成虫盘细胞增殖,并在幼虫发育末期终止细胞增殖。然而,Idgf编码基因在果蝇的其他生理过程(包括对感染的免疫反应)中的参与情况尚未完全明确。在此,我们展示了Idgf2和Idgf3在果蝇对携带或不携带共生嗜线虫致病杆菌(分别为共生或无菌线虫)的小卷蛾斯氏线虫感染的反应中的作用。我们发现,在感染共生或无菌斯氏线虫的果蝇幼虫中,Idgf2和Idgf3会上调,且Idgf2的失活赋予果蝇幼虫抵抗无菌线虫的生存优势。Idgf2的失活会诱导Imd和Jak/Stat途径,而Idgf3的失活会诱导Imd、Toll和Jak/Stat途径。我们还表明,Imd途径受体PGRP-LE的失活会在果蝇抵抗斯氏线虫感染时上调Idgf2。最后,我们证明Idgf3的失活会诱导幼虫血细胞响应斯氏线虫而募集。我们的结果表明,Idgf2和Idgf3可能参与果蝇抗线虫免疫反应中不同但关键的免疫功能。类似的发现将促进物种特异性害虫控制策略新靶点的开发。

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