{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE345nnn/GSE345214/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Caenorhabditis elegans"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE345214"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Ectopic expression of the germline transcription factor LSL-1 contributes to developmental delay following failed maternal epigenetic reprogramming","description":"Proper development requires mechanisms that prevent germline genes from being expressed in non-germline tissues. In this study, we investigated how the germline transcription factor LSL-1 contributes to developmental defects caused by failed maternal epigenetic reprogramming in Caenorhabditis elegans. We found that LSL-1 becomes ectopically expressed in somatic tissues of spr-5; met-2 mutants and that depletion of LSL-1 partially rescues their developmental delay. RNA-seq analyses showed extensive overlap between MES-4- and LSL-1-dependent transcriptional programs and revealed that ectopic lsl-1 expression itself depends on MES-4. These findings identify LSL-1 as a downstream effector of MES-4 that promotes aberrant germline-associated transcription and developmental delay.","dates":{"publication":"2026/09/04"},"accession":"GSE345214","cross_references":{"GSM":["GSM9999609","GSM9999618","GSM9999619","GSM9999616","GSM9999617","GSM9999614","GSM9999615","GSM9999612","GSM9999613","GSM9999610","GSM9999611","GSM9999620"],"GPL":["32326"],"GSE":["345214"],"taxon":["Caenorhabditis elegans"]}}