Epigenetic memory in plants

Abstract

Epigenetics refers to heritable changes in patterns of gene expression that occur without alterations in DNA sequence. The epigenetic mechanisms involve covalent modifications of DNA and histones, which affect transcriptional activity of chromatin. Since chromatin states can be propagated through mitotic and meiotic divisions, epigenetic mechanisms are thought to provide heritable 'cellular memory'. Here, we review selected examples of epigenetic memory in plants and briefly discuss underlying mechanisms.

Keywords: epialleles; epigenetics; memory; plants; transposons.

Figure 1. Schematic illustration of parental imprinting

In females, the central cell DME removes DNA methylation from maternally expressed genes, MEA and FIS2, and from the paternally expressed gene PHE1. DNA methylation at these loci is maintained in the male gametophyte. During fertilization, the central cell fuses with one sperm cell to form the endosperm. In endosperm, maternal alleles of MEA and FIS2 are expressed. The PRC2 complex including MEA and FIS2 binds to the promoter of the paternal allele of MEA and mediates silencing by catalyzing H3K27 tri-methylation. Another unknown repressor (R) may be required for repression of the paternal allele of MEA. The PRC2 complex mediates silencing of the maternal allele of PHE. In addition to the PRC2 complex, maternal removal of DNA methylation downstream of PHE gene is required for silencing of its maternal allele.

Figure 2. FLC regulation

FRI, PAF1, and COMPASS-like complexes are involved in activation/reset of FLC at every generation. During cold exposure, the PRC2-PHD complex and non-coding RNA COLDAIR are recruited at the nucleation region of FLC and catalyze H3K27 tri-methylation. After return to higher temperatures, PRC2-PHD associates across the entire region of FLC leading to cell-autonomous stable transcriptional silencing. After prolonged cold exposure, the number of cells in which FLC is stably silenced increases.

Figure 3. Environmentally induced genetic and epigenetic variations

Stress induces activation of transposons and epigenetic changes at various silent genomic loci, including heterochromatic regions. Activated transposons may transpose and generate genetic variation. New insertions of transposons also generate epigenetic variation in the vicinity of the new insertions. In contrast, epigenetic changes are mostly transient due to restoration of the pre-stress chromatin status. Therefore, transgenerational transmission of stress-induced epigenetic changes is very restricted.