Microbes in insect gut significantly influence host physiology. While Lepidoptera is a diverse insect order, the relationship between microbial symbiosis and host development remains elusive, especially concerning role of gut-colonizing bacteria in metamorphosis. We investigated the gut microbial diversity in Galleria mellonella throughout its life cycle using 16S rRNA amplicon sequencing. Our findings revealed a predominance of Enterococcus spp. in larvae and Enterobacter spp. in pupae. Remarkably, removing Enterococcus spp. hastened the larval-to-pupal transition. Transcriptome analysis showed an upregulation of immune response genes in pupae and hormone genes in larvae. Notably, the production of antimicrobial peptides in the host gut varied with developmental stages. Some of these peptides suppressed the growth of Enterococcus innesii, a dominant gut bacterium in G. mellonella larvae. This research underscores the pivotal role of gut microbiota shifts in metamorphosis, driven by the secretion of antimicrobial peptides in the G. mellonella digestive system.

Many insects form mutualistic relationships with microbial symbionts, crucial for their physiological processes. The bean bug, Riptortus pedestris, establishes a unique gut symbiosis with the genus Caballeronia and consistently acquires these symbionts from surrounding soil with each generation. As a result, the bean bug unavoidably consumes a variety of environmental microbes, including potential pathogens. To address this, the bean bug has developed a specialized organ in its midgut that selectively filters out non-symbiotic microbes, thereby preventing contamination of its symbiotic organ. In this study, we identified a pathogenic strain from the genus Burkholderia that lethally affects the bean bug post-invasion of the symbiotic organ. This pathogen employs a strategy of mimicking the motility of native symbionts to infiltrate the symbiont sorting organ and displays a pronounced resistance against antimicrobial agents produced by the host. Upon establishing itself in the symbiotic organ, the pathogen breaches the midgut cells, leading to host mortality, and subsequently disperses into the external environment. Our findings unveil a cunning pathogenic tactic that exploits the mimicry of native symbionts within an insect's symbiotic framework.