Abstract
Thermal stress negatively impacts crop yields, and as the overall temperature of the earth's atmosphere is gradually increasing, the identification of the temperature transduction pathway of the heat signal is essential in developing new strategies in order to adapt plant breeding to warmer climates. Heat stress damages the molecular structures and physiological processes in plants in proportion to the level and duration of the stress, which leads to different types of responses. In general, plants respond more efficiently when they are first subjected to a moderate temperature increase before being subjected to a higher temperature stress. This adaptive response is called the acclimation period and has been investigated in several plant species. However, there is a lack of information on the dynamic of the Heat Shock Response (HSR) over a continuous period of temperature rise without an acclimation period. In this paper, we investigated the effects of mild (30 °C) and high (37 °C) continuous heat stress over a 24-h period. Through RNA-Seq analysis, we assessed the remodeling of the transcriptome in the moss Physcomitrella patens. Our results showed that the 30 °C treatment particularly affected the expression of a few genes at 1 and 24 h, suggesting a biphasic response. Up-regulated genes at 1 h encode mainly HSR proteins (protein folding and endoplasmic reticulum stress), indicating an early heat response; while the up-regulated genes at 24 h belong to the thiamine biosynthesis pathway. In contrast, the genes involved in photosynthesis and carbon partitioning were repressed by this treatment. Under a higher temperature stress (37 °C), the induction of the HSR occurred rapidly (1 h) and was then attenuated throughout the time points investigated. A network approach (Weighted Gene Correlation Network Analysis, WGCNA) was used to identify the groups of genes expressing similar profiles, highlighting a HsfA1E binding motif within the promoters of some unrelated genes which displayed rapid and transient heat-activation. Therefore, it could be suggested that these genes could be direct targets of activation by a HsfA1E transcription factors.