{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328031/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328031"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"11β‑HSD2 buffers fetal glucocorticoid exposure inducing Per1 expression under maternal stress","description":"Glucocorticoids (GCs) have been proposed as maternal-fetal communication signals. However, fetal circadian rhythms are initially shielded from maternal entrainment, in addition to delayed circadian clock emergence due to CLOCK suppression. Premature CLOCK/BMAL1 activation disrupts Hes7-driven somite-like structure in gastruloids. Given the genomic proximity of Per1 to Hes7 and their transcriptional ripple effect, the physiological significance of delayed cell-autonomous circadian clock development and the temporal program of maternal-fetal communication during the developmental process have remained unclear. Here, based on a marked decline in Hsd11b2, encoding a GC-inactivating 11β-HSD2 enzyme, during organogenesis, we performed split-litter embryo-transfer experiments in which Hsd11b2 knockout (KO) and wild-type (WT) embryos shared the same maternal environment. Amniotic fluid (AF) GCs remained low and arrhythmic under basal conditions. In contrast, maternal stress caused a pronounced GC surge and Per1 induction in KO, suggesting that 11β-HSD2 buffers acute maternal GC surges. Despite the genomic proximity of Per1 to Hes7 and their transcriptional ripple effect, stress-associated and pharmacological GC exposure recapitulated no overt segmentation defects in vivo. Embryonic stem cell-derived gastruloid assays confirmed that neither GC exposure nor Per1 induction arrested Hes7 oscillations, whereas premature CLOCK/BMAL1 activation impaired these processes even in Hes7 KO gastruloid with ectopic rescue, suggesting that interference with the segmentation clock is mediated by premature CLOCK/BMAL1 activation, not by GC-induced Per1 expression. These findings clearly show that maternal GC signals are selectively buffered during early development. In addition, suppression of CLOCK/BMAL1 activity preserves segmentation clock function, indicating delayed circadian clock emergence is actively regulated during embryogenesis.","dates":{"publication":"2026/08/30"},"accession":"GSE328031","cross_references":{"GSM":["GSM9670649","GSM9670648","GSM9670647","GSM9670646","GSM9670645","GSM9670689","GSM9670655","GSM9670654","GSM9670698","GSM9670697","GSM9670653","GSM9670652","GSM9670696","GSM9670651","GSM9670695","GSM9670694","GSM9670650","GSM9670693","GSM9670692","GSM9670691","GSM9670690","GSM9670659","GSM9670658","GSM9670657","GSM9670656","GSM9670666","GSM9670665","GSM9670664","GSM9670663","GSM9670662","GSM9670661","GSM9670660","GSM9670669","GSM9670668","GSM9670667","GSM9670677","GSM9670676","GSM9670675","GSM9670674","GSM9670673","GSM9670672","GSM9670671","GSM9670670","GSM9670639","GSM9670638","GSM9670637","GSM9670636","GSM9670635","GSM9670679","GSM9670678","GSM9670688","GSM9670644","GSM9670643","GSM9670687","GSM9670642","GSM9670686","GSM9670685","GSM9670641","GSM9670640","GSM9670684","GSM9670683","GSM9670682","GSM9670681","GSM9670680"],"GPL":["34290"],"GSE":["328031"],"taxon":["Mus musculus"],"PMID":["[42703617]"]}}