RT Journal Article SR Electronic T1 Drosophila Toll links systemic immunity to long-term intestinal function JF bioRxiv FD Cold Spring Harbor Laboratory SP 248138 DO 10.1101/248138 A1 Magda L. Atilano A1 Marcus Glittenberg A1 Shivohum Bahuguna A1 Lihui Wang A1 Petros Ligoxygakis YR 2018 UL http://biorxiv.org/content/early/2018/12/20/248138.abstract AB The intestine is an organ where immune and metabolic functions are co-ordinated with tissue renewal via progenitor somatic stem cells (PSSCs). How this is achieved is still unclear. We report that in Drosophila, a generalised infection increased PSSC numbers. This was mimicked by expressing a constitutive form of the immune receptor Toll in PSSCs and blocked when Toll was silenced via RNAi. Without infection, absence of bacterial recognition and downstream Toll signalling resulted in a short lifespan and an age-dependent decrease of PSSCs and gut microbiota. The latter implied a metabolic environment incompatible with the presence of bacteria. Indeed, infection or constitutive Toll signalling in PSSCs triggered 4E-BP transcription in enterocytes, while loss of signalling reduced it. 4E-BP controlled fat levels and sustained the microbiota suggesting that Toll-dependent regulation of 4E-BP was important for long-term gut function. Therefore, the Toll pathway is crucial for responses to both infection and microbiota.