Project description:ChIP-chip of HPL-2 in met-2 set-25 C. elegans mixed-stage embryo EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: GW638; Developmental Stage: Mixed-stage Embryo; Genotype: met-2(n4256) set-25(n5021); Sex: population predominantly Hermaphrodites perhaps with some Males; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: temperature 20
Project description:We asked if the perinuclear position of chromosome arms in C. elegans depends on the histone methyltransferases MET-2 and SET-25. To this end, we performed LMN-1-DamID in wild-type (N2) and mutant (set-25 met-2) strains. LMN-1-DamID signal on chromosome arms was significantly reduced in the mutant.
Project description:Histone H3K9 trimethylation (H3K9me3) plays a pivotal role in the establishment and maintenance of heterochromatin and is essential for facilitating epigenetic inheritance. H3K9me3 is often biasedly deposited and associated with repetitive sequence region, although the underlying mechanism remain poorly understood. In this study, we identify two proteins, SECP-1 and SECP-2, as crucial cofactors for the genome-wide deposition of H3K9me3 in Caenorhabditis elegans. SECP-1 interacts directly with SECP-2 and the primary H3K9me3 methyltransferase, SET-25, forming a protein complex that bridges SECP-2 with SET-25. This complex assembles in the cytoplasm and is transported into the nucleus through SET-25. Once in the nucleus, the complex is recruited to and concentrated at SET-25’s genomic targets in an interdependent manner. The accumulation of this complex correlates with the formation of condensates at repetitive sequences, the perinuclear localization of heterochromatin, and the epigenetic inheritance of small RNA-mediated gene silencing. The introduction of transgenic arrays leads to the redistribution of the SECP-1/SECP-2/SET-25 complex to the transgene locus, a genome-wide decrease in H3K9me3 levels, and an increase in repetitive sequence expression. We propose that repetitive sequences drive the formation of condensates containing H3K9me3 methyltransferase complexes, which in turn causes a biased deposition of H3K9me3 at these genomic regions.
