Biology subjects

Strobel, K.

Publications and source records attributed to Strobel, K..

2 recordsLinked to original sources

bioRxiv2025

E(spl)m4 Directly Antagonizes Traf4 to Inhibit JNK Signaling in Drosophila

TRAF proteins are adaptor proteins that participate in signal transduction downstream of the Toll or TNF receptors and could elicit E3-Ubiquitin Ligase activity. They have been implicated in multiple processes during signal transduction, inflammation, and morphogenesis. In Drosophila, Traf4 has been implicated in the regulation of JNK signaling and cell death as well as Adherens Junctions regulation. Using overexpression approaches, we show here that Traf4 promotes JNK and caspase activation, as well as junctional E-Cadherin/ {beta}-Catenin depletion, resulting in epithelial cell delamination. Using biochemical, modelling, and functional genetics approaches, we further show that the Bearded-type small protein E(spl)m4 binds to Traf4, and inhibits its downstream signaling towards JNK activation and cell delamination, without affecting the effects of Traf4 on Adherens Junctions. Thus, this study identifies an endogenous peptide inhibiting Traf4 signaling, potentially by blocking Traf4 trimerization.

developmental biology↗

bioRxiv2025

Tumour-derived Ilp8 and Upd3 control intestinal progenitor cells depletion during cachexia in Drosophila larvae

In animals, tumour development triggers systemic effects, impacting the physiology of distant organs. In Drosophila larvae, wing disc neoplastic tumours result in developmental delay and organ wasting reminiscent of cachexia. This paraneoplastic syndrome affects many organs, but its effects on the intestine, a key organ in the regulation of nutrient and energy homeostasis, remain understudied. We describe here that neoplastic tumours also affect the development of the larval midgut, leading to altered cell type numbers, with a depletion of the stem-cell-like Adult Midgut Precursors (AMPs), and a disorganisation of the niche cells which enter precocious differentiation. Importantly, these intestinal cell type alterations are initiated before the onset of reduced food intake, and of muscle and adipose tissue atrophies, and thus represent a new paraneoplastic phenotype. Screening for mediators, we show that tumour derived Ilp8 and Upd3 control AMPs number and niche specification respectively.

developmental biology↗