{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330530/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Drosophila melanogaster"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE330530"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"An Innate Immune Receptor Toll-1 converts chronic light stress into glial-phagocytosis","description":"Chronic 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.","dates":{"publication":"2026/05/15"},"accession":"GSE330530","cross_references":{"GSM":["GSM9728229","GSM9728231","GSM9728230","GSM9728233","GSM9728232","GSM9728235","GSM9728234"],"GPL":["34457"],"GSE":["330530"],"taxon":["Drosophila melanogaster"]}}