Gut bacterial metabolism modulates developmental homeostasis in Drosophila

Abstract

Human body, consisting of about 10 trillion cells, carries about ten times as many microorganisms in intestines. Recently, the metabolic activities performed by these bacteria have attracted the attention of many researchers. But it is not easy to study this mutualism of host-bacteria interaction in human and mice, because their intestinal microorganisms was composed of too many bacteria species, and host genetic manipulation was intractable.In this regards, Drosophila melanogaster can provide a solution to these disadvantages for studying mutualism more closely. First, all gut flora were considered to be the study of mutualism due to the simple microbial communities of gut microbes Drosophila harboring. In host, germ-free flies could be easily generated and desired microorganism could be easily mono-associated to host. It is well known that genetic modification was tractable.By taking these advantages, we investigated, using Drosophila as a model system, that mutualism between Drosophila and gut bacteria, and observed that normal commensal flora was important for proper development of host, especially in growth-rate and body size, and pronounced in diet-restriction conditions. We also observed that Acetobacter pomorum, a major gut flora of Drosophila, alone could represent the microbial community in Drosophila’s normal development.In a screen for the factor of Acetobacter pomorum that engaged in host’s normal development, it is identified that the abilities of Acetobacter pomorum to oxidize ethanol were important for host’s normal development. These abilities to oxidize ethanol increase the expression of Drosophila insulin like peptides (dilps) in host’s brain, and these increased level of dilps affect to larval growth and adult body size via the metabolism of larval fat-body. Our results show that ethanol metabolism of Acetobacter pomorum was essential to normal development of host through modulating host metabolic pathway by insulin signaling in Drosophila.