GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330530/primaryOK200TranscriptomicsDrosophila melanogasterExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE330530GEOGSEfalseAn Innate Immune Receptor Toll-1 converts chronic light stress into glial-phagocytosisChronic stress can cause progressive neuronal degeneration, yet the molecular mechanisms linking stress sensing to neuroimmune responses remain elusive. In this study, using a Drosophila model of chronic light-induced stress, we show that photoreceptor neurons accumulate reactive oxygen species (ROS) and exhibit Toll-1 activation which involves Spätzle ligands and receptor endocytosis. Toll-1 activation in neurons promotes axonal degeneration by inducing expression of the glial phagocytic receptor Draper (Drpr), leading to the engulfment of stressed axons. Genetic interaction analyses indicate that Toll-1 functions upstream of Drpr in a stress-responsive signaling cascade. Blocking either Toll-1 or Drpr attenuates axon loss under light stress, while Toll-1 overexpression exacerbates it. Toll-1 also plays a similar pro-degenerative role in an activity-dependent olfactory neuron degeneration paradigm, pointing to a broader role for this mechanism in neural degeneration. Together, these findings identify a neuron-glia signaling axis that converts sustained stress into structural degeneration.2026/05/15GSE330530GSM9728229GSM9728231GSM9728230GSM9728233GSM9728232GSM9728235GSM972823434457330530Drosophila melanogaster