TAGC2020 poster_Rujuta Deshpande.pdf (32.1 MB)

The role of intestinal TOR signaling in metabolic responses to bacterial infection

Download (32.1 MB)
posted on 20.04.2020, 20:51 by Rujuta Deshpande, Andee Qiao, Savraj S. Grewal
The submission includes 1 .pfd file of the poster.

The poster is about how an organism is tolerates a pathogenic infection and the metabolic and physiological adaptations underlying it. The study uses Drosophila melanogaster as a model system to study the metabolic changes upon infection.

Upon oral infection with pathogenic bacteria, Drosophila adults mount organism-wide immune and physiological responses in order to provide infection resistance and promote tolerance. The intestine plays a central role in mediating these effects. Upon infection, damaged intestinal epithelial enterocytes (ECs) promote local stem cell-mediated regeneration to promote tissue repair. The intestine also signals to other tissues to control host metabolism and physiology.

Interestingly, we found a rapid increase in TOR kinase signalling in the intestine specific to infection stress, which was prominent in ECs, but also apparent in enteroendocrine (EE) and stem cells. TOR signaling is a well-established regulator of cellular, tissue and whole body metabolism. We therefore explored whether the intestinal TOR induction might contribute to metabolic responses to infection. We found that oral infection led to local intestinal upregulation of many lipid metabolic genes and reduced levels of whole body lipids.

Furthermore, pharmacological inhibition of TOR blocked many of the infection-mediated changes in gut lipid gene expression.

These data suggest that intestinal TOR induction may mediate both local and whole body metabolic responses to infection. EE cells secrete many different endocrine hormone peptides that can signal both locally and remotely to control metabolism, which were up-regulated upon EC specific TOR induction.

We are currently exploring whether signaling through these peptides may couple the infection induced intestinal TOR activation to host lipid metabolic changes, and how these changes may contribute to infection tolerance.



Clark H. Smith Brain Tumor Graduate Studentship


Program Number