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.

中文翻译：

---

磷壁酸的 D-丙氨酰化有助于慢性营养不良期间植物乳杆菌介导的果蝇生长。

微生物环境影响动物生理。然而，这种功能相互作用的潜在分子机制在很大程度上是不确定的。此前，我们发现在慢性营养不良期间，果蝇的主要共生伙伴植物乳杆菌菌株部分通过增强肠肽酶的表达来促进宿主幼体的生长和成熟。通过在果蝇幼虫中筛选植物乳杆菌的转座子插入文库，我们确定了一种由 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。该操纵子的缺失导致细菌细胞壁改变，磷壁酸的D-丙氨酰化完全丧失。我们证明 L. 果蝇肠细胞直接感知带有 D-丙氨酰化磷壁酸的植物细胞壁，以确保在慢性营养不良期间获得最佳的肠肽酶表达和活性、幼体生长和成熟。因此，我们得出结论，除了肽聚糖外，磷壁酸修饰还参与了肠道中发生的宿主-共生细菌分子对话。