There are 21 heat shock factor (HSF) homologs in Arabidopsis (35S

There are 21 heat shock factor (HSF) homologs in Arabidopsis (35S promoter:construct into quadruple knockout (and mutant and promoted callus formation in in tolerance to different heat stress regimes, and to hydrogen peroxide, but not to salt and osmotic stresses. stress tolerance in the future. Plants have evolved complex response systems to cope with environmental stresses. Dynamic reprogramming of transcriptional activities constitutes one of the major events that enhance stress tolerance. Several transcription factor families are involved in complex and overlapping responses under different stress conditions (Singh et al., 2002). WRKY, MYB, APETALA2/ethylene response factor, bZIP, NAC, zinc-finger proteins, and heat shock factors (HSFs) are encoded by large gene families and have been intensively studied for their functions in stress responses (Singh et al., 2002; Saibo et al., 2009; Hirayama and Shinozaki, 2010; Santos et al., 2011; Scharf et al., 2012). Among these transcription factor families, HSFs are of particular interest because their functions in heat stress response and thermotolerance are highly conserved across all eukaryotes. HSFs are characterized by a DNA-binding domain name and hydrophobic heptad repeat regions (Wu, 1995; Morimoto, 1998; ?kerfelt et al., 2010). Current models suggest that in higher eukaryotes, common HSFs assemble into an active, trimeric conformation via the hydrophobic heptad repeat regions in response to stress factors (?kerfelt et al., 2010; Anckar and Sistonen, 2011). The trimerized transcription factors bind to the conserved heat shock cis-elements (GAAnnTTC) in the promoters of target genes via the DNA-binding domains and further recruit transcription machineries for gene expression. During nonstress or poststress periods, HSF activity is usually negatively regulated by attenuators such as HEAT SHOCK PROTEIN70 (HSP70), HSP90, and HSF binding protein (HSBP) or modulated by posttranslational modifications such as phosphorylation, acetylation, and sumoylation (Morimoto, 1998; Satyal et al., 1998; Pirkkala et al., 2001; ?kerfelt et al., 2010; Xu et al., 2012). In contrast to yeast (genes in the A1 group, and and both constitute pairs of duplicated genes diverged after a recent whole genome duplication event (Blanc et al., 2003). Studies on quadruple knockout (KO) and four triple KO mutants showed that this four A1-type HSFs have overlapping functions in the development of seeds and cotyledons and HSFA1a, HSFA1b, or HSFA1d alone, but not HSFA1e, could trigger heat stress response and confer thermotolerance (Liu et al., 2011; Yoshida et al., 2011). The triple KO of and the quadruple KO (are the grasp regulators of heat stress response in Arabidopsis. In addition, tolerance to salt, osmotic, and oxidative stresses were compromised in the mutant (Liu et al., 2011), suggesting that HSFA1s function under a broad range of adverse conditions that are not limited to heat stress. The functions of individual HSFA1s in response to the stress factors other than heat have not been decided. In response to elevated temperature, HSFA1s trigger a transcriptional cascade by inducing the expression of diverse transcription regulators, including HSFs of other classes (class A2, A3, A7, B1, and B2), DREB2A, DREB2B, MBF1C, and bZIP28 (Liu et al., 2011; Yoshida et al., 2011; Liu and Charng, 2012). Several of these transcription regulators have been shown to be involved in heat stress response and thermotolerance (Sakuma et al., 2006; Charng et al., 2007; Gao et al., 2008; Larkindale and Vierling, 2008; Schramm et al., 2008; Suzuki et al., 2008; Yoshida et al., 2008; Ikeda et al., 2011). The heat inducibility of the HSFs is usually a feature unique to plants and is not found in yeast and animals (Nover et al., 2001; von Koskull-D?ring et al., 2007), and of TSC2 the HSFs, HSFA2 is the most highly induced upon heat stress (Busch et al., 2005). In Arabidopsis and tomato (mutant and examined whether ectopic HSFA2 expression BAY 61-3606 could rescue the defects of the mutant in development and stress tolerance under various conditions. Interestingly, complete or partial recovery from multiple defects was BAY 61-3606 observed in the transgenic plants, suggesting that HSFA2 can at least partially replace the function of the HSFA1s. However, it could not rescue the defect of the mutant under salt or osmotic stresses. Genes preferentially activated by HSFA1 or HSFA2 upon heat stress were identified by microarray analysis of the transcriptomes of the wild type, (the transfer DNA KO mutant of mutant, and the mutant transformed with recombinant (Mutant in Growth and Development To examine whether and to what extent HSFA2 functions in the absence of the HSFA1s, we generated transgenic lines BAY 61-3606 made up of a recombinant complementary DNA fused to the 35S promoter in the mutant background. Four transgenic lines, designated as and the in different transgenic lines as determined by reverse transcription (RT)-PCR to confirm their genotypes. Under normal conditions, transcripts of were detected in all the transgenic lines, but not in the wild type and mutant, indicating the constitutive expression of the transgene. and lines had high and low expression levels of in transgenic plants overexpressing HSFA2. RT-PCR analysis of the transcript levels of under normal conditions in 7-d-old seedlings of wild-type (W), mutant, … The growth and morphologies of the transgenic plants readily manifested the effect of.

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