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Abstract
Transposable elements (TEs), the movement of which can damage the genome, are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in the sperm companion cell - vegetative cell (VC) - of the flowering plant Arabidopsis thaliana. However, the extent and mechanism of this activation are unknown. Here we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed DNA demethylation. We further demonstrate that DEMETER access to some of these TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent mechanism. We demonstrate that H1 is required for heterochromatin condensation in plant cells and show that H1 overexpression creates heterochromatic foci in the VC progenitor cell. Taken together, our results demonstrate that the natural depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation, heterochromatin relaxation, and TE activation.
Highlights
Large proportions of most eukaryotic genomes are comprised of transposable elements (TEs), mobile genetic fragments that can jump from one location to another
We identified 114 TEs that are transcribed at significantly higher levels in pollen than rosette leaves, and likely to be activated in the vegetative cell (VC) (Figure 1—source data 1) (Slotkin et al, 2009)
Given the well-demonstrated role of DNA methylation at the transcriptional start site (TSS) for transcriptional suppression (Barau et al, 2016; Eichten et al, 2012; Hollister and Gaut, 2009; Manakov et al, 2015; Meng et al, 2016), our data demonstrate that DME-mediated demethylation in the VC is the primary cause of TE activation
Summary
Large proportions of most eukaryotic genomes are comprised of transposable elements (TEs), mobile genetic fragments that can jump from one location to another. Eukaryotic hosts have evolved efficient epigenetic mechanisms, including DNA methylation, to suppress TEs (He et al, 2011; Law and Jacobsen, 2010). Recent studies point to episodes of TE activation that occur in specific cell types and/or particular developmental stages (Garcia-Perez et al, 2016; Martınez and Slotkin, 2012). These TE activation events provide unique opportunities to understand epigenetic silencing mechanisms, and the co-evolution between TEs and their hosts
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