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Lack of single amino acids transcriptionally tunes sensory systems to enhance microbiota intake

ABSTRACT: Maintaining sufficient levels of Amino acids (AAs) from the diet is essential for the organism to maintain protein translation and other metabolic processes. Amazingly, the removal of even a single eAA from the diet is sufficient to induce an increase of proteinaceous food intake in Drosophila melanogaster. This process of turning a physiological “need” for any eAA into a psychological “want” driving proteinaceous-food search and consumption still remains poorly understood. Moreover, dietary manipulations of different eAAs have varying effects on metabolism and physiology which depend on the specific eAA depleted. Thus, a systemic analysis of single eAAs effects on the organism is needed. To achieve that, we sequenced RNA from fly heads following exposure to diets depleted of single AAs. We found that depletion of eAAs had different impacts on transcription, however a significant number of regulated transcripts were shared across deprivations, indicating common mechanisms of response to deprivation. Surprisingly chemosensory receptor genes were found amongst the consistently diet-modulated genes, in spite of minimal, if any, change in sensory environment. Genetic manipulations of Or92a confirm its importance for the acceptance of the appropriate food sources, namely , yeast. While Ir76a governs approaches to specific gut bacteria. These results expand the idea that metabolic-internal state can alter sensory processing already at the transcriptional level, regardless of the sensory environment. Our work uncovers common and unique transcriptional changes induced by all eAA deprivations and reveals novel mechanisms underlying the organism’s behavioral and physiological response to dietary challenges.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE270723 | GEO | 2025/10/27

REPOSITORIES: GEO

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Project description:Animals can thrive on variable food resources as a result of autonomous processes and beneficial relationships with their gut microbes. Food intake elicits major physiological changes, which are compensated with transient systemic responses that maintain homeostasis in the organism. This integration of external information occurs through cellular sensory elements, such as nuclear receptors, which modulate gene expression in response to specific cues. Given the importance of the germline stem cells (GSCs) for the development of the germ line and the continuity of the species, it is reasonable to assume that GSCs might be shielded from the negative influence of environmental perturbations. To our knowledge, however, there are no mechanisms reported that protect proliferating germ cells from harmful dietary metabolites. Using Caenorhabditis elegans as a model, we report that the somatic activity of the conserved nuclear receptor nhr-114/HNF4 protects GSC divisions and GSC integrity from dietary metabolites. In the absence of nhr-114 and on certain bacterial diets, otherwise somatically normal animals accumulate germ cell division defects during development and become sterile. We find that in nhr-114(-) animals the induction of germline defects and sterility depends on the bacterial metabolic status with respect to the essential amino acid tryptophan. This illustrates an animal-microbe interaction in which somatic nuclear receptor activity preserves the germline by buffering against dietary metabolites, likely through a somatic detoxifying response. Overall, our findings uncover an unprecedented and presumably evolutionary conserved soma-to-germline axis of communication that maintains reproductive robustness on variable food resources. Trasncriptional profiles of adult sterile nhr-114(RNAi) animals were compared to those of sterile glp-1(q224ts) animals. Independently, the transcriptional profiles of wild type animals fed an OP50 diet supplemented with Tryptophan was compared to wild type animals fed a standard OP50 diet.

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Lack of single amino acids transcriptionally tunes sensory systems to enhance microbiota intake

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