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一种内寄生蜂会影响宿主的 DNA 甲基化。

An endoparasitoid wasp influences host DNA methylation.

机构信息

Department of Bioresource Sciences, Andong National University, Andong 36729, Korea.

出版信息

Sci Rep. 2017 Feb 23;7:43287. doi: 10.1038/srep43287.

DOI:10.1038/srep43287
PMID:28230192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5322367/
Abstract

Parasitism by endoparasitoid wasps changes the expression of various host genes, and alters host immune and developmental processes. However, it is not clearly understood how parasitism changes host gene expression in a whole genome scale. This study focused on an epigenetic control of Cotesia plutellae, an endoparasitoid wasp, against its host, Plutella xylostella. Two DNA methyltransferases (DNMT-1 and DNMT-2) are encoded in the genome of P. xylostella. In addition, methyl-binding domain proteins (MBDs) and DNA demethylation factor, ten-eleven translation protein (TET) are encoded. DNA methylation of P. xylostella genomic DNA was confirmed by restriction digestion with Gla I specific to 5-methylcytosine. DNA methylation intensity in parasitized (P) larvae was decreased compared to that in nonparasitized (NP) larvae, especially at late parasitic stage, at which expression levels of both DNMT-1 and DNMT-2 were also decreased. DNA demethylation of P. xylostella was confirmed in both NP and P larvae by restriction digestion with PvuRts1I recognizing 5-hydroxymethyl cytosine. Parasitism also suppressed expression levels of TET and MBDs. Treatment of 5-aza-2'-deoxycytidine (AZA) reduced DNA methylation intensity of NP larvae, causing suppression of hemocyte-spreading behavior and delay of immature development. RNA interference of DNMT-1 or DNMT-2 mimicked the adverse effects of AZA.

摘要

内寄生蜂通过寄生改变了各种宿主基因的表达，并改变了宿主的免疫和发育过程。然而，寄生如何在全基因组范围内改变宿主基因表达还不是很清楚。本研究集中研究了小菜蛾内寄生蜂 Cotesia plutellae 的一种表观遗传控制，以对抗其宿主小菜蛾。小菜蛾基因组中编码了两种 DNA 甲基转移酶（DNMT-1 和 DNMT-2）。此外，还编码了甲基结合域蛋白（MBD）和 DNA 去甲基化因子 ten-eleven 翻译蛋白（TET）。通过用特异性识别 5-甲基胞嘧啶的 Gla I 进行限制酶切，证实了小菜蛾基因组 DNA 的 DNA 甲基化。与非寄生（NP）幼虫相比，寄生（P）幼虫的 DNA 甲基化强度降低，尤其是在晚期寄生阶段，此时 DNMT-1 和 DNMT-2 的表达水平也降低。通过用识别 5-羟甲基胞嘧啶的 PvuRts1I 进行限制酶切，证实了 NP 和 P 幼虫中的 DNA 去甲基化。寄生还抑制了 TET 和 MBD 的表达水平。5-氮杂-2'-脱氧胞苷（AZA）处理降低了 NP 幼虫的 DNA 甲基化强度，导致血细胞扩散行为受到抑制，不成熟发育延迟。DNMT-1 或 DNMT-2 的 RNA 干扰模拟了 AZA 的不利影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/166902355583/srep43287-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/db2de22107f6/srep43287-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/1ac13610cdb4/srep43287-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/639aad5076fa/srep43287-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/aecd353225b9/srep43287-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/4b01b0f1d2be/srep43287-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/9854cf42d58f/srep43287-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/7530730114bf/srep43287-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/23769c29ce7e/srep43287-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/7812b2e36f5a/srep43287-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/166902355583/srep43287-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/db2de22107f6/srep43287-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/1ac13610cdb4/srep43287-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/639aad5076fa/srep43287-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/aecd353225b9/srep43287-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/4b01b0f1d2be/srep43287-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/9854cf42d58f/srep43287-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/7530730114bf/srep43287-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/23769c29ce7e/srep43287-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/7812b2e36f5a/srep43287-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d2/5322367/166902355583/srep43287-f10.jpg

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