Core Genome Responses Involved in Acclimation to High Temperature

Abstract

Plants can acclimate rapidly to environmental conditions, including high temperatures. To identify molecular events important for acquired thermotolerance, we compared viability and transcript profiles of Arabidopsis thaliana treated to severe heat stress (45°C) without acclimation or following two different acclimation treatments. Notably, a gradual increase to 45°C (22°C to 45°C over 6 h) led to higher survival and to more and higher-fold transcript changes than a step-wise acclimation (90 min at 38°C plus 120 min at 22°C before 45°C). There were significant differences in the total spectrum of transcript changes in the two treatments, but core components of heat acclimation were apparent in the overlap between treatments, emphasizing the importance of performing transcriptome analysis in the context of physiological response. In addition to documenting increases in transcripts of specific genes involved in processes predicted to be required for thermotolerance (i.e. protection of proteins and of translation, limiting oxidative stress), we also found decreases in transcripts (i.e. for programmed cell death, basic metabolism, and biotic stress responses), which are likely equally important for acclimation. Similar protective effects may also be achieved differently, such as prevention of proline accumulation, which is toxic at elevated temperatures and which was reduced by both acclimation treatments but was associated with transcript changes predicted to either reduce proline synthesis or increase degradation in the two acclimation treatments. Finally, phenotypic analysis of T-DNA insertion mutants of genes identified in this analysis defined eight new genes involved in heat acclimation, including cytosolic ascorbate peroxidase and the transcription factors HsfA7a (heat shock transcription factor A7a) and NF-X1.

The Heat-Inducible Transcription Factor HsfA2 Enhances Anoxia Tolerance in Arabidopsis

“…The heat + anoxia treatment up-regulated 702 genes that were not regulated by either heat or anoxia. Several of these genes were found to be heat regulated under various experimental conditions (35% when comparing our results with the data set of Larkindale and Vierling [2008]), while others were also actually modulated by either heat or anoxia in our experiments, although the statistical significance of their change in expression did not pass the threshold used to select differentially regulated genes. Analysis of data using MapMan (Thimm et al, 2004;Fig.…”

Extensive Rearrangement of the Arabidopsis Mitochondrial Genome Elicits Cellular Conditions for Thermotolerance

“…Stress-responsive transcription factors such as NF-X1, involved in heat acclimation (Larkindale and Vierling, 2008), WRKY, involved in pathogen defense signaling (for review, see Eulgem and Somssich, 2007), and DREB2B, responsive to desiccation and high-salinity stress (Nakashima et al, 2000), were up-regulated. Temperature-induced lipocalin, involved in scavenging harmful lipophilic molecules and thought to participate in plant responses to heat and cold stress (Chi et al, 2009), was prominent in the double mutant under normal growth conditions.…”

Understanding the molecular events underpinning cultivar differences in the physiological performance and heat tolerance of cotton (Gossypium hirsutum)

“…The short-term heat shock response is characterised by the synthesis of heat shock proteins (HSPs) (Malik et al 1999;Hong and Vierling 2000;Nieto-Sotelo et al 2002;Busch et al 2005) and heat shock transcription factors (Mishra et al 2002;Panchuk et al 2002;Ogawa et al 2007;Kant et al 2008;Larkindale and Vierling 2008;Yokotani et al 2008). Initial induction of genes encoding heat stress transcription factors and HSPs is accompanied by alteration of genes associated with protein biosynthesis, folding and processing (Busch et al 2005;Hewezi et al 2008;Larkindale and Vierling 2008;Yokotani et al 2008) and protein degradation (Rizhsky et al 2002;Hewezi et al 2008;Kant et al 2008;Tian et al 2009).…”

“…Initial induction of genes encoding heat stress transcription factors and HSPs is accompanied by alteration of genes associated with protein biosynthesis, folding and processing (Busch et al 2005;Hewezi et al 2008;Larkindale and Vierling 2008;Yokotani et al 2008) and protein degradation (Rizhsky et al 2002;Hewezi et al 2008;Kant et al 2008;Tian et al 2009). Increases in respiration are associated with the upregulation of genes encoding proteins involved in the catabolism of assimilates and glycolysis (Rizhsky et al 2002;Kant et al 2008;Larkindale and Vierling 2008).…”

“…Molecular analysis indicates that the heat response is complex and varied, involving significant changes in global gene expression (Rizhsky et al 2004;Busch et al 2005;Rensink et al 2005;Kant et al 2008;Larkindale and Vierling 2008) and multigene interactions (Humphreys and Humphreys 2005). The initial heat stress response occurs within the first 0.5-1 h (Busch et al 2005;Kant et al 2008) after exposure to temperatures exceeding the thermal kinetic window that permits normal enzyme function in plants (Burke et al 1988) but may vary between species.…”