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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0258

Promoter and gene body methylation dynamics in late gestation

PROMOTER AND GENE BODY METHYLATION DYNAMICS IN LATE GESTATION

In late gestation, promoter and gene body regions become hypermethylated with increasing gestational age but are enriched in different pathways, with the major epigenetic transition occurring between 32 and 36 weeks.

The study aimed to compare methylation trajectories in promoter and gene body regions in neonates exposed to threatened preterm labor (TPL), assess the functional pathways associated with these region-specific changes, identify temporal inflection points in late gestation, and relate methylation dynamics to neurodevelopmental processes. Dried blood spot samples from 99 neonates exposed to TPL (55 males, 44 females; gestational age 23–37 weeks, mean 30.4 ± 3.2 weeks) were analyzed using the Illumina Infinium MethylationEPIC BeadChip. CpGs were classified as promoter (3,273 CpGs, 2,396 genes) or gene body (4,693 CpGs, 3,001 genes); associations between gestational age (GA) and methylation were assessed for each compartment using rank-based regression with false discovery rate (FDR) correction. Gene Ontology enrichment analysis was performed using GeneCodis3. Promoter CpGs showed hypermethylation with increasing gestational age and were enriched in pathways related to morphogenesis, extracellular matrix organization, and sensory system development. Gene body CpGs also became hypermethylated with increasing gestational age but were enriched in pathways related to axon guidance, synaptic activity, neurotransmitter transport, and calcium signaling. The major epigenetic transition occurred between 32 and 36 weeks of gestation, coinciding with rapid cortical folding and thalamocortical connectivity. The authors suggest that these patterns indicate the sequential silencing of developmental programs (promoters) and the strengthening of connectivity programs (gene bodies), that promoter hypermethylation stabilizes tissue architecture while gene body methylation supports neural circuit formation, and that these dynamics may inform the identification of early biomarkers of neurodevelopmental risk in preterm infants.

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