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果蝇抗寄生蜂免疫反应中的孔形成毒素样蛋白

Pore-Forming Toxin-Like Proteins in the Anti-Parasitoid Immune Response of Drosophila.

作者信息

Magyar Lilla B, Ábrahám Edit, Lipinszki Zoltán, Tarnopol Rebecca L, Whiteman Noah K, Varga Viktória, Hultmark Dan, Andó István, Cinege Gyöngyi

机构信息

Innate Immunity Group, Institute of Genetics, HUN-REN Biological Research Centre, Szeged, Hungary.

Doctoral School of Biology, University of Szeged, Szeged, Hungary.

出版信息

J Innate Immun. 2025;17(1):10-28. doi: 10.1159/000542583. Epub 2024 Dec 3.

DOI:10.1159/000542583
PMID:39626640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11731912/
Abstract

INTRODUCTION

Species of the ananassae subgroup of Drosophilidae are highly resistant to parasitoid wasp infections. We have previously shown that the genes encoding cytolethal distending toxin B (CdtB) and the apoptosis inducing protein of 56 kDa (AIP56) were horizontally transferred to these fly species from prokaryotes and are now instrumental in the anti-parasitoid immune defense of Drosophila ananassae. Here we describe a new family of genes, which encode proteins with hemolysin E domains, heretofore only identified in prokaryotes. Hemolysin E proteins are pore-forming toxins, important virulence factors of bacteria.

METHODS

Bioinformatical, transcriptional, and protein expressional studies were used.

RESULTS

The hemolysin E-like genes have a scattered distribution among the genomes of species belonging to several different monophyletic lineages in the family Drosophilidae. We detected structural homology with the bacterial Hemolysin E toxins and showed that the origin of the D. ananassae hemolysin E-like genes (hl1-38) is consistent with prokaryotic horizontal gene transfer. These genes encode humoral factors, secreted into the hemolymph by the fat body and hemocytes. Their expression is induced solely by parasitoid infection and the proteins bind to the developing parasitoids.

CONCLUSIONS

Hemolysin E-like proteins acquired by horizontal gene transfer and expressed by the primary immune organs may contribute to the elimination of parasitoids, as novel humoral factors in Drosophila innate immunity.

摘要

引言

果蝇科阿纳纳萨果蝇亚组的物种对寄生蜂感染具有高度抗性。我们之前已经表明,编码细胞致死膨胀毒素B(CdtB)和56 kDa凋亡诱导蛋白(AIP56)的基因是从原核生物水平转移到这些果蝇物种中的,并且现在在果蝇的抗寄生蜂免疫防御中发挥作用。在这里,我们描述了一个新的基因家族,其编码的蛋白质具有溶血素E结构域,迄今为止仅在原核生物中发现。溶血素E蛋白是形成孔道的毒素,是细菌重要的毒力因子。

方法

采用生物信息学、转录和蛋白质表达研究。

结果

溶血素E样基因在果蝇科几个不同单系谱系的物种基因组中呈分散分布。我们检测到与细菌溶血素E毒素的结构同源性,并表明果蝇溶血素E样基因(hl1 - 38)的起源与原核生物水平基因转移一致。这些基因编码体液因子,由脂肪体和血细胞分泌到血淋巴中。它们的表达仅由寄生蜂感染诱导,并且这些蛋白质与发育中的寄生蜂结合。

结论

通过水平基因转移获得并由主要免疫器官表达的溶血素E样蛋白,作为果蝇先天免疫中的新型体液因子,可能有助于消除寄生蜂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/9b937b90a14e/jin-2025-0017-0001-542583_F08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/7a5ab0e1f93e/jin-2025-0017-0001-542583_F01.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/9ce6cdf7f9a3/jin-2025-0017-0001-542583_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/c31d6ad07997/jin-2025-0017-0001-542583_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/e574545a2871/jin-2025-0017-0001-542583_F06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/0b9683eb6cc4/jin-2025-0017-0001-542583_F07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/9b937b90a14e/jin-2025-0017-0001-542583_F08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/7a5ab0e1f93e/jin-2025-0017-0001-542583_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/f0ca37469ad3/jin-2025-0017-0001-542583_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/2481fa4e2252/jin-2025-0017-0001-542583_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/9ce6cdf7f9a3/jin-2025-0017-0001-542583_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/c31d6ad07997/jin-2025-0017-0001-542583_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/e574545a2871/jin-2025-0017-0001-542583_F06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/0b9683eb6cc4/jin-2025-0017-0001-542583_F07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0928/11731912/9b937b90a14e/jin-2025-0017-0001-542583_F08.jpg

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