Background. Stress affects host growth and development and can induce changes in the gut microbiome, commonly defined as dysbiosis. Dysbiosis has been proposed to affect community beta-diversity and within-beta-diversity (community dispersion). As abiotic and biotic stresses, nutrient restriction (NR) also impairs host fitness and results in dysbiosis. However, NR does not introduce overt negative effectors or selectors, such as toxic compounds, pathogens, or parasites, resulting in its role as a determinant of beta-diversity changes being questioned. We hypothesize that following NR, gut dysbiosis is reflected via changes in networking properties of the microbiome rather than via variation in its beta-diversity and/or dispersion. To test our hypothesis, we fed the black soldier fly, Hermetia illucens, a nutritionally versatile polyphagous insect, with two NR diets and a control full-nutrient (FN) diet. Then, we assessed the effects of NR on insect growth and development and gut physicochemical conditions to validate the presence of dysbiosis. In addition, we analyzed the bacterial diversity associated with larvae, pupae, and adults via 16S rRNA gene sequencing to assess the role of NR on the composition, structure, and stability of the bacterial communities.
Results. NR strongly affected insect growth and development, inducing significant changes in the physiochemical conditions of the larval gut. Further, diet-dependent differences in bacterial composition—expected in holometabolous/polyphagous insects—were observed, with enrichment in diet-specific keystone bacterial taxa (Bacilli in FN-fed individuals and Clostridia and Gamma- and Alphaproteobacteria in NR-fed individuals), and greater microbiome dispersion in adults but not in larvae and pupae.
Conclusions. While NR establishes alternative stable configurations of the gut microbiome compared with normally fed gut, NR-driven dysbiotic growth performance is considerably reflected in rarefied, less structured, and connected bacterial interactomes than in within beta-diversity changes.