Parental S-adenosylmethionine diet defines offspring immune response via histone H3K4me3 complex and Endoplasmic Reticulum UPR.

ABSTRACT: S-adenosylmethionine (SAM), is a ubiquitous cofactor necessary for methyltransferase reactions. Deficiency in SAM results in dysregulation of crucial methylation and cellular dysfunction. SAM promotes innate immunity via histone H3K4me3 complex, raising the question of whether SAM supplementation in the parental generation could be reprogrammed histone modifications in offspring and thereby affect the innate immunity of descendants. In this study, we fed Caenorhabditis elegans with SAM, which led to enhance innate immunity. Furthermore, this enhancement is capable of transmitting the phenotype to subsequent generations. Transcriptome sequencing and GO functional enrichment analysis revealed that SAM induced the expression of genes involved in immune responses and IRE-1-mediated endoplasmic

SUBMITTER: Liu F 

PROVIDER: S-EPMC12462273 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature