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\b[<plants> establish <epigenetic states> through sequence- and context-dependent recruitment, maintain selected states through replication and regulatory feedback, and erase others when development requires a reset.] These processes protect repetitive DNA, stabilize cell identity and coordinate developmental or environmental responses. An <epigenetic state> is therefore regulated information, not simply a collection of chemical marks that always switch genes off.
<plant> <DNA methylation> occurs in CG, CHG and CHH contexts, where H denotes A, C or T. The contexts have overlapping but distinct control mechanisms. At a methylated CG dyad, <DNA replication> initially produces hemimethylated daughter DNA; <MET1> helps restore methylation on the new strand. This provides a direct route for maintaining an existing pattern. By contrast, asymmetric <CHH methylation> cannot be retained merely by copying an equivalent methylated cytosine across a symmetric dyad: continued targeting by small-RNA or <chromatin> pathways is required. <CHG methylation> is strongly coupled to histone recognition and reinforcing <chromatin> feedback rather than being explained by CG maintenance alone.
For establishment at many repeats, canonical <RNA-directed DNA methylation> provides sequence specificity. <Pol IV> produces precursors that, with <RDR2>, generate double-stranded RNA; <DCL3> processes these into 24-nucleotide <small interfering RNAs>. An <Argonaute> such as <AGO4> uses guide information in association with nascent scaffold transcripts made by <Pol V>, helping recruit <DRM2> to the matching locus. <DRM2> can establish methylation in multiple cytosine contexts. Thus <transcription> can paradoxically be required to establish transcriptional silencing: the scaffold supplies a locus-specific interaction surface rather than representing productive expression of the silenced gene.<Pol IVb and Pol V noncoding-transcription study by Andrzej T. Wierzbicki and others>[Pol V scaffold transcription and its requirement alongside siRNA production]{ref}
Maintenance is also reinforced by interactions between DNA and histone states. <CMT3> recognizes <H3K9me2>-associated <chromatin> and contributes to <CHG methylation>. Histone methyltransferases including <SUVH4>, <SUVH5> and <SUVH6> couple methylated DNA to H3K9 methylation, forming a reinforcing relationship. <CMT2> contributes strongly to <CHH methylation> in heterochromatic regions, while <RdDM> is particularly important in other targeted contexts. Mutant methylomes show both specialization and redundancy, as well as dependencies linking non-CG methylation, small RNAs and H3K9 states.<Non-CG methylation patterns shape the epigenetic landscape in Arabidopsis by Hume Stroud and others>[methyltransferase mutants, CMT2 activity and dependencies between epigenetic pathways]{ref} These are interacting pathways, not three enzymes independently copying three unrelated codes.
Accessibility is an essential part of the mechanism. Dense <nucleosomes> and linker histones can restrict a methyltransferase even when an appropriate DNA sequence is present. <DDM1> remodels H1-containing <heterochromatin> to allow access, complementing RNA-directed targeting in different <chromatin> environments.<The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin by Assaf Zemach and others>[heterochromatin accessibility and complementary methylation pathways]{ref} This explains why maintenance can depend on both an enzyme that writes a modification and machinery that permits the enzyme to reach its substrate.
Histone-based developmental memory is a distinct layer. <Polycomb repressive complex 2> deposits <H3K27me3> at selected developmental loci. Sequence-specific regulators, transcriptional context and environmental signals determine where recruitment occurs; recycling of parental histones and restoration of modifications help preserve selected states after replication. Yet the presence of a histone mark does not prove that the mark autonomously copies itself or is sufficient for inheritance. Recruitment, feedback, <nucleosome> turnover and the transcriptional state all need to be considered. H3K27-based silencing of developmental genes should also be distinguished from H3K9-associated transposon <heterochromatin>.
<vernalization> illustrates how a state is established for a purpose and maintained for a limited interval. In <Arabidopsis thaliana>, prolonged cold promotes stable repression of the floral repressor <FLC>, allowing later flowering in appropriate conditions. Natural accessions differ in the cold exposure needed for stable silencing, correlated with accumulation of <H3K27me3>.<Variation in the epigenetic silencing of FLC contributes to natural variation in Arabidopsis vernalization response by Chikako Shindo and others>[variation in stable FLC silencing and H3K27me3 after different cold exposures]{ref} Maintaining the state after warming allows the <plant> to retain information about winter rather than respond only to the instantaneous temperature.
Erasure is equally important. Active <DNA demethylation> can involve DNA glycosylase/lyase activity followed by repair that replaces methylated bases. The identification of <ROS1> connected promoter demethylation to protection against inappropriate gene silencing.<ROS1 gene-silencing study by Zhizhong Gong and others>[ROS1 mutant phenotype and methylated-DNA glycosylase activity]{ref} Reproductive reprogramming is cell-type specific: <DEMETER> has a maternal role in imprinting and seed viability, rather than representing indiscriminate erasure in every cell.<DEMETER, a DNA glycosylase domain protein, is required for endosperm gene imprinting and seed viability in Arabidopsis by Yeonhee Choi and others>[maternal gametophyte function, imprinting and seed phenotype]{ref}
An environmentally acquired state may also need resetting between generations. The vernalized <FLC> state is normally reset during reproduction and seed development, so the offspring can require its own winter. Perturbing the histone demethylase <ELF6> impaired resetting and allowed inheritance of a partially vernalized state.<Epigenetic reprogramming that prevents transgenerational inheritance of the vernalized state by Pedro Crevillén and others>[FLC resetting and ELF6-dependent H3K27 demethylation]{ref} This contrasts with loci whose methylation states remain stable through reproduction. <plants> cannot be described either as preserving every acquired mark or as globally erasing all epigenetic information.
\Image[/past-exam-of-the-plant-sciences-course-of-the-university-of-cambridge/2024/paper-pll1-epigenetic-states.png]
{title=Original overview of DNA methylation establishment, reinforcing maintenance, active demethylation and a distinct Polycomb developmental-memory pathway}
Why retain these systems? Silencing mobile and repetitive DNA limits genome damage, <chromatin> states help cells maintain appropriate expression despite a shared genome, and developmental memory coordinates events separated in time. Selective reprogramming supports gametes and seeds, while boundaries and active demethylation prevent necessary silencing from spreading into genes that must function. Methylation within an expressed gene is not equivalent to repression at a promoter, and a transient transcriptional response is not automatically an inherited state. \b[<plant> epigenetic control is therefore a balance of targeting, faithful persistence and timely erasure, with different mechanisms serving different biological intervals and genomic contexts.]
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