Cold priming uncouples light- and cold-regulation of gene expression in Arabidopsis thaliana
Abstract Background The majority of stress-sensitive genes responds to cold and highlight in the same direction, if plants face the stresses for the first time. As shown recently for a small selection of genes of the core environmental stress response cluster, pre-treatment of Arabidopsis thaliana with a 24 h long 4 °C cold stimulus modifies cold regulation of gene expression for up to a week at 20 °C, although the primary cold effects are reverted within the first 24 h. Such memory based regulation is called priming. Here, we show the effect of 24 h cold priming on cold regulation of gene expression on a transcriptome-wide scale and test if and how cold priming effects light regulation of gene expression. Results 304 genes were differently regulated between cold-primed and non-primed plants after a second 24 h long 4 °C cold treatment. After triggering the plants with a heat-filtered highlight stimulus (800 µmol quanta m -2 s -1 ), 1011 genes showed priming dependent regulation. Only 32 of the priming-sensitive genes responded similarly to cold and light triggering. The majority of the priming-sensitive genes were regulated in a stressor-specific manner. 29 genes were even inversely regulated by the two triggering stimuli. Cold priming preferentially supported expression of genes involved in the defense against plant pathogens upon cold triggering. The regulation took place on the cost of the expression of genes involved in growth regulation and transport. On the contrary, cold priming resulted in stronger expression of genes regulating metabolism and development and weaker expression of defense genes in response to highlight triggering. qPCR in several independently cultivated and treated samples confirmed the trends observed by RNA-Sequencing. Conclusion The 24 h long priming cold stimulus activates a several day lasting stress memory that controls cold and light regulation of gene expression and adjusts growth and defense regulation in a stressor-specific manner.