Plant epigenetics

Plant epigenetics investigates changes in gene activity associated with regulatory states such as DNA methylation and chromatin organization, including states that persist through mitosis or reproduction. Stable expression differences need not be caused by a changed DNA sequence, but independence from sequence variation must be tested.

The Karma epiallele connects this distinction to agriculture: reduced methylation of an intronic retrotransposon was associated with altered splicing and the low-yield mantled form of tissue-cultured oil palm. Somaclonal variation can thus involve a regulatory change as well as a sequence mutation.^[ref]

Persistence is a measurable property. Comparisons of Arabidopsis thaliana lines descended from a common ancestor found many changes at individual methylated positions but greater stability across larger methylated regions. Calling every transient response an epimutation would obscure this difference.^[ref]

An Arabidopsis thaliana gene whose ectopic expression and flowering phenotype can be associated with a stably unmethylated promoter state.

A tomato vitamin E biosynthetic gene whose expression can be influenced by methylation of a nearby promoter retrotransposon.

A prior stimulus changes the response to a subsequent challenge. Persistence may involve metabolites, proteins, regulatory feedback or chromatin; priming alone does not establish epigenetic inheritance.

HSFA2 is a heat-shock transcriptional regulator involved in sustained stress responses in Arabidopsis thaliana. Its role in somatic stress memory can outlast its direct occupancy of target regions.

Experiments found transient association of HSFA2 with memory-related loci together with longer-lasting histone methylation and altered responses to a subsequent heat exposure. The distinction between the initial response and later memory is crucial: HSFA2 dependence of the latter does not imply dependence of every immediate heat response.^[ref]

Persistence of a response state within an individual after the initial stimulus has ended, distinguished from inheritance through reproduction.

Vernalization is acquisition of the capacity to flower following prolonged cold. In Arabidopsis thaliana, persistent silencing of the floral repressor FLC helps retain information about winter after temperatures rise.

The memory's lifetime differs from its acquisition. Experiments on resetting between generations show why an individual plant can remember cold while its descendants still need their own cold exposure. Perennial plants can use different seasonal reactivation patterns, as illustrated by PEP1 in Arabis alpina.^[ref][ref]

The Arabis alpina FLC orthologue, whose seasonal reactivation contributes to perennial flowering behavior.

FLOWERING LOCUS C, or FLC, encodes a floral repressor in Arabidopsis thaliana. Prolonged cold can establish a persistently silenced state, connecting chromatin regulation to the memory underlying vernalization.

Natural variation in FLC silencing contributes to differences in cold requirements. Measuring later flowering and the persistence of repression tests memory, whereas measuring expression only during cold does not establish that the regulatory change survives warming.^[ref]

Epigenetic silencing of one parental set of ribosomal RNA genes in a hybrid; it is not simply the deletion of those genes.

RNA-directed DNA methylation, or RdDM, is a plant regulatory pathway in which small RNAs guide methylation of homologous DNA. Canonical components include Pol IV, RDR2, DCL3 and Pol V, connecting production of small RNAs with recognition of target chromatin.

Noncoding transcription can supply scaffold transcripts at the target, rather than serving only to produce a protein. Experiments on specialized polymerases showed how this transcriptional activity participates in silencing adjacent or overlapping regions.^[ref]

Targeted alteration of an epigenetic state, distinguished from cutting or rewriting the target DNA sequence. Persistence after removal of the targeting factor is locus dependent.

An association analysis relating epigenomic measurements to a phenotype. Association alone does not establish causal direction or independence from genetic variation.

A line from a mapping population segregating experimentally induced epigenetic differences in a comparatively uniform genetic background. New transposon insertions and residual sequence differences still need to be assessed.

An alternative regulatory state of a locus associated with an epigenetic difference. Its stability and independence from DNA sequence variation must be tested.

A gain or loss of an inherited epigenetic state rather than a change in nucleotide sequence.