SRA

Heat stressed Arabidopsis plants release heterochromatin-associated transposable element (TE) silencing, which however is not accompanied by major reductions of epigenetic repressive modifications. In this study, we explored the functional role of histone H1 in repressing heterochromatic TEs in response to heat stress. Loss of H1 caused activation of pericentromeric GYPSY elements upon heat treatment, despite that these elements remained highly methylated. In contrast, non-pericentromeric COPIA elements became activated concomitantly with loss of DNA methylation. The same COPIA elements became activated in heat-treated chromomethylase2 (cmt2) mutants, indicating that H1 represses COPIA elements through maintaining DNA methylation under heat. We discovered that H1 is required for TE repression in response to heat stress, but its functional role differs depending on TE location. Strikingly, H1 deficient plants treated with the DNA methyltransferase inhibitor zebularine were highly tolerant to heat stress, suggesting that both, H1 and DNA methylation redundantly suppress the plant response to heat stress. Overall design: We generated and analyzed RNA and bisulfite-sequencing data of wild-type, h1, and cmt2 mutant seedlings before and after heat stress.