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有益共生菌通过下调肽聚糖识别蛋白的表达来促进果蝇生长。

Beneficial commensal bacteria promote Drosophila growth by downregulating the expression of peptidoglycan recognition proteins.

作者信息

Gallo Marialaura, Vento Justin M, Joncour Pauline, Quagliariello Andrea, Maritan Elisa, Silva-Soares Nuno F, Battistolli Matteo, Beisel Chase L, Martino Maria Elena

机构信息

Department of Comparative Biomedicine and Food Science, University of Padova, Padova, Italy.

Department of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, USA.

出版信息

iScience. 2022 May 5;25(6):104357. doi: 10.1016/j.isci.2022.104357. eCollection 2022 Jun 17.

DOI:10.1016/j.isci.2022.104357
PMID:35601912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9121327/
Abstract

Commensal bacteria are known to promote host growth. Such effect partly relies on the capacity of microbes to regulate the host's transcriptional response. However, these evidences mainly come from comparing the transcriptional response caused by commensal bacteria with that of axenic animals, making it difficult to identify the animal genes that are specifically regulated by beneficial microbes. Here, we employ associated with to understand the host genetic pathways regulated by beneficial bacteria and leading to improved host growth. We show that microbial benefit to the host relies on the downregulation of peptidoglycan-recognition proteins. Specifically, we report that bacterial proliferation triggers the lower expression of PGRP-SC1 in larval midgut, which ultimately leads to improved host growth and development. Our study helps elucidate the mechanisms underlying the beneficial effect exerted by commensal bacteria, defining the role of immune effectors in the relationship between Drosophila and its gut microbes.

摘要

已知共生细菌可促进宿主生长。这种效应部分依赖于微生物调节宿主转录反应的能力。然而,这些证据主要来自于将共生细菌引起的转录反应与无菌动物的转录反应进行比较,这使得难以确定由有益微生物特异性调节的动物基因。在这里,我们利用……来了解由有益细菌调节并导致宿主生长改善的宿主遗传途径。我们表明,微生物对宿主的益处依赖于肽聚糖识别蛋白的下调。具体而言,我们报告细菌增殖会触发幼虫中肠中PGRP-SC1的表达降低,最终导致宿主生长和发育得到改善。我们的研究有助于阐明共生细菌发挥有益作用的潜在机制,确定免疫效应分子在果蝇与其肠道微生物关系中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/9c5119f3055a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/59a32398ee3c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/51fcc531c4bc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/845ad1079dd8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/a81385a706fe/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/9c5119f3055a/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/59a32398ee3c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/51fcc531c4bc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/845ad1079dd8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/a81385a706fe/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff7a/9121327/9c5119f3055a/gr4.jpg

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