Saez-Carrion, E. | Search bioRxiv

bioRxiv2026

Tumour rewires host tryptophan metabolism to promote organism-wide immune suppression

How tumour genotype reshapes systemic metabolism to drive immune tolerance and tumour progression remains unclear. Here, we show that Pten-deficient Drosophila tumours reprogram host tryptophan metabolism, triggering systemic and local changes in immune and stromal compartments to foster tolerance. Tumour-derived nitric oxide activates the kynurenine pathway in liver-like tissue, selectively increasing the 3-hydroxykynurenine (3-HK) branch. Host 3-HK promotes tumour progression and suppresses immune function via aryl hydrocarbon receptor (AhR) signalling. These results identify the kynurenine pathway as a central tumour-host nexus and reveal how tumour genotype creates immune vulnerabilities.

cancer biology↗

bioRxiv2022

Neuroendocrine control of catch-up growth in Drosophila

Children and other vertebrate animals stunted due to malnutrition can compensate for this deficit by resuming growth at a higher-than-normal rate via a still ill-defined mechanism. High mortality and adverse effects later in life may offset the positive effects of catch-up growth. Here we report that the invertebrate Drosophila melanogaster also experiences catch-up growth following a period of starvation, and the relaxin receptor Lgr4 instigates this catch-up growth. Starved larvae compensate for weight loss by growing two or more times faster and starting maturation within the same time as the non-starved sibling by preventing a rise in insulin-like growth (IGF)-induced ecdysone under Lgr4 control. Our data reveal that catch-up growth is associated with a surge of insulin, not IGF, which may clarify how catch-up growth often leads to metabolic problems and obesity.

developmental biology↗