epigenetics

H3K4me3

associated with active promoters

sits on unmethylated CpG islands

bivalent domains

regions of embryonic stem cell DNA that include both activating (H3K4me3) and repressive marks (H3K27me3)

H3K4me1

associated with active regulatory regions (enhancers)

H3K27me3, H4K20me

repressive histone tail modifications

H3K9me3

classically repressive in promoter region of gene and promotes DNA methylation

can be found in the coding region of an active genes

H3K9ac

higher at the GR promoter in high LG/ABN offspring

H3K56ac

sits at the DNA entry-exit site

allows DNA breathing without collapse

dyad axis

area of strongest histone-DNA contact

H3K64ac, H3K122ac, H3T118ph

associated with strong destabilization of DNA at dyad axis

H4K91ac

residue found in the histone-histone interface

modification destabilizes the octamer

H3K79me

found in the outer surface histone-histone interface

associated with active transcription and creates a docking site

acetylation, methylation, phosphorylation, ubiquitylation

4 most common histone modifications

HAT

histone acetyltransferase

HDAC

histone deacetylases

H3

histone that most commonly exhibits modifications on its residues

writer

an enzyme that adds a modification to a histone

eraser

an enzyme that removes a modification from a histone

readers

proteins (sometimes enzymes) that directly bind to histone modifications carry out further effects

bromodomains of reader

binds acetylated lysine modification

14-3-3 reader

binds phosphorylated serine modification

ING2

reader protein that binds to H3K4me3 and flips meaning of modification by binding HDAC complex

glucocorticoid receptor

receptors found in the hippocampus that when activated downregulate the HPA

NGFI-A

transcription factor for GR gene

exon 1₇

exon of GR gene that contains NGFI-A binding site

often found in particular transcripts of the gene associated with high maternal care

site 16

CpG site that serves as the 5’ binding site of NGFI-A on exon 1₇

site 17

CpG site that serves as the 3’ binding site of NGFI-A on exon 1₇

HP1

reader with chromodomain that binds H3K9me

BPTF/NURF complex

reader of H3K4me3 that promotes chromatin remodeling

JMJD2A

binds H3K4me3 and is a histone lysine demethylase

CHD1

binds H3K4me and is a chromatin-remodeling ATPase

H3K36me3

found at the 3’ end of a gene, promotes transcription

has a negative effect when located at the promoter of a gene

PC2

reader for H3K27me3

WDR5

reader for H3K4me1

ADD domain

binds unmethylated H3K4

found in DNMT3L

CXXC

binds unmethylated CpG sites of DNA

PWWP domain

binds H3K36me3

found in DNMT3a

SRA domain

binds hemimethylated DNA

tudor/chromo/BAH domains

bind methylated H3K9

PHD domain

binds methylated H3K4

MBD domain

binds methylated CpG sites of DNA

CFP1

binds unmethylated CpG sites and promotes H3K4 methylation

JHDM1

binds unmethylated CpG sites and demethylates H3K36

PHF8

binds methylated H3K4 and demethylates nearby repressive histone marks

UHRF1

potential mechanism for copying histone marks after DNA replication

restriction enzymes

enzymes cut either only methylated or only unmethylated sites

affinity enrichment

antibody or methyl-binding protein pulls down methylated DNA

whole genome bisulfite conversion (WGBS)

bisulfite conversion of entire genome producing methylation state of every CpG

reduced representation bisulfite sequencing (RRBS)

bisulfite conversion of CpG-rich regions of genome only

methylation array

bisulfite conversion of a large number of pre-chosen CpG sites

ChIP-seq

histone modification identification by antibody targeting after cross-linking and shearing DNA

cut and run

ChIP-exo

DamID

DNase-seq

DNase I cuts euchromatin, isolating active promoters and enhancers

ATAC-seq

transposase cuts DNA and adds primers in open chromatin regions

Hi-C

cross links proximal DNA regions and sequence both halves

ATAC-Me

bisulfite conversion and ATAC → methylation is read on open DNA

NOMe-seq

enhancer

distally promotes target gene transcription

insulator

marks gene domain edges by blocking enhancer contact with other genes

CTCF / cohesin