We needed to block the hypermethylation building up in peri/centromeres. Our genetic attempts hit roadblocks, so we switched to a pharmacological approach: 5-Aza, a DNA methylase inhibitor.
Remarkably, 5-Aza not only boosted ROS1-induced resistance to Pst-Lux, it prolonged the immune memory!
7/9

ROS1 caused widespread demethylation and small RNA loss in chromosome arms, *but* in the highly repetitive pericentromeric/centromeric regions we saw the opposite — increases in DNA methylation and small RNAs.
5/9

Bursts of ROS1 activity robustly induced resistance against the pathogenic bacteria Pst-Lux and the oomycete pathogen Hpa.

This immune memory, generated by ROS1, lasted 1-2 weeks, providing an ideal system to study both the establishment and erasure of immune memory.

3/9

In Arabidopsis, the removal of an epigenetic mark, DNA methylation, often occurs in response to pathogen infection or abiotic stress.
We used an estradiol-inducible gene construct for the DNA demethylase ROS1 to transiently increase demethylation activity in plants.
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