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H3K4me3 is used as a histone code or histone mark in epigenetic studies (usually identified through chromatin immunoprecipitation) to identify active gene promoters. H3K4me3 promotes gene activation through the action of the NURF complex, a protein complex that acts through the PHD finger protein motif to remodel chromatin. [2]
H3K4me1 is a chromatin signature of enhancers, H3K4me2 is highest toward the 5′ end of transcribing genes and H3K4me3 is highly enriched at promoters and in poised genes. H3K27me3 , H4K20me1 and H3K4me1 silence transcription in embryonic fibroblasts, macrophages, and human embryonic stem cells (ESCs).
During development, TrxG proteins maintain activation of required genes, particularly the Hox genes, after maternal factors are depleted. [8] This is accomplished by preserving the epigenetic marks, specifically H3K4me3, established by maternally-supplied factors. [9]
However, patterns were discovered including a set of 17 histone modifications that are present together at over 3000 genes. [16] Mass spectrometry -based top-down proteomics has provided more insight into these patterns by being able to discriminate single molecule co-occurrence from co-localization in the genome or on the same nucleosome. [ 17 ]
The H3K27me3 mark silences the gene while the H3K4me3 mark allows the gene to not be permanently silenced, and activated when needed. [2] Embryonic stem cells and imprinted genes are associated with both activating (H3K4me3) and repressive (H3K27me3) marks, as they allow a gene to be repressed until activation is needed.
The gene targeting method in knockout mice uses mouse embryonic stem cells to deliver artificial genetic material (mostly of therapeutic interest), which represses the target gene of the mouse by the principle of homologous recombination. The mouse thereby acts as a working model to understand the effects of a specific mammalian gene.
This is the case in H3K27ac which is an active enhancer mark. It is found in distal and proximal regions of genes. It is enriched in transcriptional start sites (TSS). H3K27ac shares a location with H3K27me3 and they interact in an antagonistic manner. H3K27me3 is often seen to interact with H3K4me3 in bivalent domains . [11]
H3K4me3-promoters; H3K4me1- primed enhancers; H3K36me3-gene bodies; H3K27me3-polycomb repression; H3K9me3-heterochromatin; The human genome was annotated with chromatin states. These annotated states can be used as new ways to annotate a genome independently of the underlying genome sequence.