Differential Regulation of Immune Signaling and Survival Response in Drosophila melanogaster Larvae upon Steinernema carpocapsae Nematode Infection.
Differential Regulation of Immune Signaling and Survival Response in Drosophila melanogaster Larvae upon Steinernema carpocapsae Nematode Infection.
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DOI：
10.3390/insects9010017
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发表时间：
2018-02-08
期刊：
影响因子：
3
通讯作者：
Eleftherianos I
中科院分区：
文献类型：
--
作者：
Yadav S;Gupta S;Eleftherianos I
果蝇是研究天然抗病原体免疫反应的分子组成和途径的极好模型。线虫寄生虫Steinernema carpocapsae和它的共生细菌Xellichabdus cereophila形成一种复合体，对昆虫具有高致病性，包括D。黑腹菌我们使用了共生（携带X。无菌性（X.嗜线虫的免疫信号通路基因的调控。黑腹幼虫，并评估某些突变体对这些病原体的生存反应。我们发现，这两种类型的S。carpocapsae上调MyD 88（Toll），但不上调PGRP-LE（Imd）; carpocapsae强烈上调Wengen（Jnk）、Domeless（Jak/Stat）、Dawdle（TGFβ，Activin）和Decapentaplegic（TGFβ，BMP）。我们进一步发现，失活的Wengen和Decapentaplegic赋予了一个生存优势的幼虫感染纯S。carpocapsae，而突变的PGRP-LE促进感染共生线虫的幼虫的存活。
Drosophila melanogaster is an excellent model to dissect the molecular components and pathways of the innate anti-pathogen immune response. The nematode parasite Steinernema carpocapsae and its mutualistic bacterium Xenorhabdus nematophila form a complex that is highly pathogenic to insects, including D. melanogaster. We have used symbiotic (carrying X. nematophila) and axenic (lacking X. nematophila) nematodes to probe the regulation of genes belonging to different immune signaling pathways in D. melanogaster larvae and assess the survival response of certain mutants to these pathogens. We found that both types of S. carpocapsae upregulate MyD88 (Toll), but not PGRP-LE (Imd); whereas axenic S. carpocapsae strongly upregulate Wengen (Jnk), Domeless (Jak/Stat), Dawdle (TGFβ, Activin), and Decapentaplegic (TGFβ, BMP). We further found that inactivation of Wengen and Decapentaplegic confers a survival advantage to larvae infected with axenic S. carpocapsae, whereas mutating PGRP-LE promotes the survival of larvae infected with symbiotic nematodes.
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