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磷壁酸的 D-丙氨酸化有助于慢性营养不良期间植物乳杆菌介导的果蝇生长。

D-Alanylation of teichoic acids contributes to Lactobacillus plantarum-mediated Drosophila growth during chronic undernutrition.

机构信息

Institut de Génomique Fonctionnelle de Lyon (IGFL), Université de Lyon, Ecole Normale Supérieure de Lyon, CNRS UMR 5242, Université Claude Bernard Lyon 1, 69364, Lyon Cedex 07, France.

Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, 78350, Jouy-en-Josas, France.

出版信息

Nat Microbiol. 2017 Dec;2(12):1635-1647. doi: 10.1038/s41564-017-0038-x. Epub 2017 Oct 9.

DOI:10.1038/s41564-017-0038-x
PMID:28993620
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5706638/
Abstract

The microbial environment influences animal physiology. However, the underlying molecular mechanisms of such functional interactions are largely undefined. Previously, we showed that during chronic undernutrition, strains of Lactobacillus plantarum, a major commensal partner of Drosophila, promote host juvenile growth and maturation partly through enhanced expression of intestinal peptidases. By screening a transposon insertion library of Lactobacillus plantarum in gnotobiotic Drosophila larvae, we identify a bacterial cell-wall-modifying machinery encoded by the pbpX2-dlt operon that is critical to enhance host digestive capabilities and promote animal growth and maturation. Deletion of this operon leads to bacterial cell wall alteration with a complete loss of D-alanylation of teichoic acids. We show that L. plantarum cell walls bearing D-alanylated teichoic acids are directly sensed by Drosophila enterocytes to ensure optimal intestinal peptidase expression and activity, juvenile growth and maturation during chronic undernutrition. We thus conclude that besides peptidoglycan, teichoic acid modifications participate in the host-commensal bacteria molecular dialogue occurring in the intestine.

摘要

微生物环境会影响动物的生理机能。然而,这种功能相互作用的潜在分子机制在很大程度上还没有得到明确。此前,我们发现,在慢性营养不良期间,植物乳杆菌(Drosophila 的主要共生伙伴)的某些菌株通过增强肠道肽酶的表达,部分促进了宿主的幼体生长和成熟。通过对无菌果蝇幼虫的植物乳杆菌转座子插入文库进行筛选,我们确定了 pbpX2-dlt 操纵子编码的细菌细胞壁修饰机制,该机制对于增强宿主消化能力和促进动物生长和成熟至关重要。该操纵子的缺失会导致细菌细胞壁发生改变,彻底丧失了磷壁酸的 D-丙氨酸化。我们表明,带有 D-丙氨酸化磷壁酸的植物乳杆菌细胞壁被果蝇肠细胞直接感知,以确保在慢性营养不良期间,肠内肽酶的最佳表达和活性、幼体生长和成熟。因此,我们得出结论,除了肽聚糖,磷壁酸的修饰也参与了发生在肠道中的宿主共生菌分子对话。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/6b7697aa5ebe/emss-74069-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/cc0c58fc29e6/emss-74069-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/fd2ff789a7c0/emss-74069-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/410c5af130fe/emss-74069-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/7671b88818c1/emss-74069-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/6b7697aa5ebe/emss-74069-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/cc0c58fc29e6/emss-74069-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/fd2ff789a7c0/emss-74069-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/410c5af130fe/emss-74069-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/7671b88818c1/emss-74069-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c51/5706638/6b7697aa5ebe/emss-74069-f005.jpg

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