After an episode of heat stress plants retain a cellular "memory" of this event, a phenomenon known as thermomemory. This mechanism allows plants to better cope against a subsequent heat event. Thermomemory occurs through the persistence of heat shock proteins (HSPs) synthesized after the first "priming" event. Maintenance of this thermomemory comes at the cost to growth though, therefore it is vital that the memory is reset when no longer required. Recently, it has been reported that autophagy is important for resetting the thermomemory. It has also been shown recently that in response to heat, Arabidopsis displays an increase in chloroplast free calcium concentration which is partially dependent on calcium sensing receptor (CAS) protein. It is not known what the purpose of this heat-activated calcium signal is. Therefore, we compared downstream responses to heat in wild type (WT) and cas mutants, as the latter produce a reduced chloroplast calcium signal to heat. We found that after thermopriming the cas mutants displayed a greater biomass and a reduced level of the small heat shock protein HSP 17.6 degradation compared to WT. cas mutants did not show an increase in free amino acid levels after thermopriming, suggesting reduced autophagy. These results suggest that heat-induced chloroplast calcium elevation is a positive signal for resetting of the thermomemory.
Keywords: Autophagy; CAS; Calcium; Chloroplast; Heat; Thermomemory.
Crown Copyright © 2021. Published by Elsevier GmbH. All rights reserved.