Figure 2.

Summary of mechanisms of heat stress memory.

The top panel illustrates the three stages detailed in (a)–(c). (a) Before HS, HSFA1 proteins are retained in the cytosol by chaperone proteins (HSP). Memory genes are inactive and the chromatin around them is dense in nucleosomes and poor in histone H3K4 methylation. (b) During HS, chaperone proteins release HSFA1 proteins. Free HSFA1 translocates to the nucleus and activates a set of heat stress-responsive genes, including HSFA2. HSFA2 binds the promoter regions of memory genes and sustains activation of their transcription. HSFA2 binding to memory genes also triggers H3K4 methylation of the neighbouring nucleosomes. Concomitantly, a chromatin remodeling complex that includes FGT1, BRM, CHR11 and CHR17 targets the TSS of memory genes to reduce nucleosome occupancy. (c) Up to several days after a HS, memory genes are primed. In absence of HSFA2 binding, the chromatin around memory genes is still enriched in H3K4 methylation, and shows low nucleosome occupancy. Thus, memory genes show a sustained expression and/or will be more quickly re-induced if another HS happens.