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通过RNA干扰敲低髓样分化因子88(MyD88)可阻止细菌对管虫变态的刺激。

MyD88 knockdown by RNAi prevents bacterial stimulation of tubeworm metamorphosis.

作者信息

Darin Emily, Farrell Morgan V, Ali Tatyana N, Rivera Alfaro Josefa, Malter Kyle E, Shikuma Nicholas J

机构信息

Department of Biology and Viral Information Institute, San Diego State University, San Diego, CA 92182.

出版信息

Proc Natl Acad Sci U S A. 2025 Jun 10;122(23):e2505805122. doi: 10.1073/pnas.2505805122. Epub 2025 Jun 2.

DOI:10.1073/pnas.2505805122
PMID:40455987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12167997/
Abstract

Diverse animals across the tree of life undergo the life-history transition of metamorphosis in response to bacteria. Although immunity has been implicated in this metamorphosis in response to bacteria, no functional connection has yet been demonstrated between immunity and metamorphosis. We investigated a host-microbe interaction involving a marine tubeworm, , that undergoes metamorphosis in response to , a metamorphosis-inducing marine bacterium. By creating a marine bacteria-mediated RNA interference approach, we show that myeloid differentiation factor 88 (MyD88), a critical immune adaptor for Toll-like receptor and interleukin pathways, is necessary for the stimulation of metamorphosis in response to bacteria. In addition to a developmental role, we show that MyD88 is necessary for survival during exposure to the bacterial pathogen , showing that utilizes MyD88 during both development and an immune response. These results provide a functional characterization of the innate immune system involved in an animal's metamorphosis.

摘要

生命之树上的各种动物会因细菌而经历变态这种生活史转变。尽管免疫作用已被认为与这种因细菌引发的变态有关,但免疫与变态之间尚未证明存在功能联系。我们研究了一种宿主 - 微生物相互作用,涉及一种海洋管虫,它会因一种诱导变态的海洋细菌而发生变态。通过创建一种海洋细菌介导的RNA干扰方法,我们表明髓样分化因子88(MyD88),一种Toll样受体和白细胞介素途径的关键免疫衔接蛋白,对于响应细菌刺激变态是必需的。除了具有发育作用外,我们还表明MyD88在暴露于细菌病原体期间对于生存是必需的,这表明在发育和免疫反应过程中都利用了MyD88。这些结果提供了参与动物变态的先天免疫系统的功能特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/ba42b05476c3/pnas.2505805122fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/238ca8d14822/pnas.2505805122fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/cd15529dff40/pnas.2505805122fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/2d099b74b71f/pnas.2505805122fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/36600990ba3f/pnas.2505805122fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/e35781323cfa/pnas.2505805122fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/ba42b05476c3/pnas.2505805122fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/238ca8d14822/pnas.2505805122fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/cd15529dff40/pnas.2505805122fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/2d099b74b71f/pnas.2505805122fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/36600990ba3f/pnas.2505805122fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/e35781323cfa/pnas.2505805122fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33da/12167997/ba42b05476c3/pnas.2505805122fig06.jpg

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