Project description:Adaptive plasticity in stress responses is a key element of plant survival strategies. For instance, moderate heat stress (HS) primes a plant to acquire thermotolerance, which allows subsequent survival of more severe HS conditions. Acquired thermotolerance is actively maintained over several days (HS memory) and involves the sustained induction of memory-related genes. We find FORGETTER3/ HEAT SHOCK TRANSCRIPTION FACTOR A3 (FGT3/HSFA3) to be specifically required for physiological HS memory and maintaining high memory-gene expression during the days following a HS exposure. HSFA3 mediates HS memory by direct transcriptional activation of memory-related genes after return to normal growth temperatures. HSFA3 binds HSFA2, and in vivo both proteins form heteromeric complexes with additional HSFs. Our results indicate that only complexes containing both HSFA2 and HSFA3 efficiently promote transcriptional memory by promoting histone H3 lysine 4 (H3K4) hyper-methylation. In summary, our work defines the major HSF complex controlling transcriptional memory and elucidates the in vivo dynamics of HSF complexes during somatic stress memory.
Project description:Plants often experience recurrent stressful events, for example during heat waves. They can adapt to such recurrent heat stress (HS), allowing subsequent survival of more severe HS conditions. At certain genes HS induces sustained expression for several days beyond the actual HS. This transcriptional memory is associated with hyper-methylation of histone H3 lysine 4 (H3K4me3), however, how this is maintained for extended periods of time is unclear. Here, we determined histone turnover by measuring chromatin association of a HS-induced histone H3.3. Genome-wide Histone turnover was not homogenous, in particular, H3.3 was retained longer at HS memory genes compared to HS-induced non-memory genes during the memory phase. While low nucleosome turnover retained H3K4 methylation, its loss did not affect turnover, suggesting that low nucleosome turnover sustains H3K4 methylation (and not vice versa). Together, our results unveil the modulation of histone turnover as a mechanism to retain environmentally-mediated epigenetic modifications.
