The Dream and MEC Complexes reinforce SPR-5; MET-2 maternal reprogramming to maintain the Germline-Soma distinction [lin-35 RNAseq]

ABSTRACT: Proper regulation of tissue-specific gene expression is essential for cell fate determination and development. In Caenorhabditis elegans, the distinction between germline and somatic cell fates is partially established through maternally inherited histone modifications. During gametogenesis, germline genes acquire transcription-coupled chromatin marks such as histone methylation, which are inherited by the zygote and must be reprogrammed at fertilization to prevent inappropriate germline gene expression in somatic tissues. This maternal reprogramming is mediated by histone-modifying enzymes, including the demethylase SPR-5/LSD1 and the H3K9 methyltransferase MET-2/SETDB1. Together, these enzymes limit DNA accessibility to transcriptional machinery, thereby resetting the chromatin landscape in te newly formed zygote. Failure to reprogram inherited histone methylation, as in spr-5; met-2 mutants, results in the ectopic expression of MES-4-targeted germline genes in somatic tissues, leading to developmental delay and sterility. Here, we investigated whether transcriptional repressor complexes—the DREAM and MEC NuRD complexes—cooperate with SPR-5 and MET-2 to specify germline versus soma. Loss of DREAM or MEC NuRD components alone causes somatic expression of germline genes. Strikingly, combined loss with spr-5; met-2 enhances developmental arrest at the L1 stage and exacerbates germline gene misexpression. By re analyzing previous published ChIP-seq data, we confirmed direct binding of MEP-1 and LIN-35 to these misregulated genes. Our findings demonstrate that maternal reprogramming and conserved chromatin repressor complexes act synergistically to repress germline transcription in somatic tissues, ensuring proper somatic development and preventing soma-to-germline transformation.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE303062 | GEO | 2025/07/19

REPOSITORIES: GEO