Abstract
Plants as sessile organisms can adapt to environmental stress to mitigate its adverse effects. As part of such adaptation they maintain an active memory of heat stress for several days that promotes a more efficient response to recurring stress. We show that this heat stress memory requires the activity of the FORGETTER1 (FGT1) locus, with fgt1 mutants displaying reduced maintenance of heat-induced gene expression. FGT1 encodes the Arabidopsis thaliana orthologue of Strawberry notch (Sno), and the protein globally associates with the promoter regions of actively expressed genes in a heat-dependent fashion. FGT1 interacts with chromatin remodelers of the SWI/SNF and ISWI families, which also display reduced heat stress memory. Genomic targets of the BRM remodeler overlap significantly with FGT1 targets. Accordingly, nucleosome dynamics at loci with altered maintenance of heat-induced expression are affected in fgt1. Together, our results suggest that by modulating nucleosome occupancy, FGT1 mediates stress-induced chromatin memory.
Highlights
Abiotic stress is a major threat to global crop yields and this problem is likely to be exacerbated in the future
We have reported the identification of the A. thaliana orthologue of Strawberry notch (Sno), FGT1, as a regulator of sustained gene induction after heat stress (HS)
We identified FGT1 from an unbiased mutagenesis screen for factors that are required for the maintenance of high HSA32::LUC expression after HS, but not for its initial induction
Summary
Abiotic stress is a major threat to global crop yields and this problem is likely to be exacerbated in the future. Priming has been described in response to pathogen attack, heat stress (HS), drought, and salt stress (Charng et al, 2006; Conrath, 2011; Jaskiewicz et al, 2011; Ding et al, 2012; Sani et al, 2013). Transcript levels were already lower at the earliest time point measured (immediately after the end of ACC), suggesting that the remodelers were necessary for full induction of these genes. This was not correlated with a reduced level of acquired thermotolerance in our assays (Figure 6—figure supplement 1)
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