Diversity in DNA recognition by heat shock transcription factors (HSFs) from model organisms

Enoki, Yasuaki; Sakurai, Hiroshi

doi:10.1016/j.febslet.2011.04.014

Cited by 20 publications

(15 citation statements)

References 23 publications

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“…Our model captures critical features of the HSF/HSE interaction that are lost with simpler computational models, namely the interdependencies between the sub-binding sites of each HSF monomer. Consistent with our model, a series of in vitro experiments with S. cerevisiae , D. melanogaster , A. thaliana , H. sapien and D. rerio HSFs indicate that HSF from each of these species can bind to discontinuous HSEs containing canonical pentamers that contain intervening five base pair gaps [36], [37]; interestingly, however, C. elegans HSF strictly binds to continuous HSEs that do not contain gaps [36]. The complex interactions between positions within a binding site are a critical aspect of inferring whether a polymorphism or mutation affects TF binding.…”

Section: Discussionsupporting

confidence: 81%

Accurate Prediction of Inducible Transcription Factor Binding Intensities In Vivo

et al. 2012

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DNA sequence and local chromatin landscape act jointly to determine transcription factor (TF) binding intensity profiles. To disentangle these influences, we developed an experimental approach, called protein/DNA binding followed by high-throughput sequencing (PB–seq), that allows the binding energy landscape to be characterized genome-wide in the absence of chromatin. We applied our methods to the Drosophila Heat Shock Factor (HSF), which inducibly binds a target DNA sequence element (HSE) following heat shock stress. PB–seq involves incubating sheared naked genomic DNA with recombinant HSF, partitioning the HSF–bound and HSF–free DNA, and then detecting HSF–bound DNA by high-throughput sequencing. We compared PB–seq binding profiles with ones observed in vivo by ChIP–seq and developed statistical models to predict the observed departures from idealized binding patterns based on covariates describing the local chromatin environment. We found that DNase I hypersensitivity and tetra-acetylation of H4 were the most influential covariates in predicting changes in HSF binding affinity. We also investigated the extent to which DNA accessibility, as measured by digital DNase I footprinting data, could be predicted from MNase–seq data and the ChIP–chip profiles for many histone modifications and TFs, and found GAGA element associated factor (GAF), tetra-acetylation of H4, and H4K16 acetylation to be the most predictive covariates. Lastly, we generated an unbiased model of HSF binding sequences, which revealed distinct biophysical properties of the HSF/HSE interaction and a previously unrecognized substructure within the HSE. These findings provide new insights into the interplay between the genomic sequence and the chromatin landscape in determining transcription factor binding intensity.

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Section: Discussionsupporting

confidence: 81%

Accurate Prediction of Inducible Transcription Factor Binding Intensities In Vivo

et al. 2012

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“…This indicates that the transcriptional memory response is controlled by cis-regulatory elements in the 5 0 -promoter and that neither 3 0 nor genic sequences are required. This promoter fragment contains two canonical heat shock elements (HSEs) that may bind HSFs (Schramm et al, 2006;Enoki and Sakurai, 2011;Jung et al, 2013). A binding site of HSFA2 in this region was determined in vitro and in vivo (Schramm et al, 2006;L€ amke et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Distinct heat shock factors and chromatin modifications mediate the organ‐autonomous transcriptional memory of heat stress

et al. 2018

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Plants can be primed by a stress cue to mount a faster or stronger activation of defense mechanisms upon subsequent stress. A crucial component of such stress priming is the modified reactivation of genes upon recurring stress; however, the underlying mechanisms of this are poorly understood. Here, we report that dozens of Arabidopsis thaliana genes display transcriptional memory, i.e. stronger upregulation after a recurring heat stress, that lasts for at least 3 days. We define a set of transcription factors involved in this memory response and show that the transcriptional memory results in enhanced transcriptional activation within minutes of the onset of a heat stress cue. Further, we show that the transcriptional memory is active in all tissues. It may last for up to a week, and is associated during this time with histone H3 lysine 4 hypermethylation. This transcriptional memory is cis-encoded, as we identify a promoter fragment that confers memory onto a heterologous gene. In summary, heat-induced transcriptional memory is a widespread and sustained response, and our study provides a framework for future mechanistic studies of somatic stress memory in higher plants.

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“…Heat shock transcription factors (Hsfs) are the central regulators in the plant's cellular response to HS (Nover et al, 2001;von Koskull-Döring et al, 2007). They bind to a heat shock element (HSE) composed of continuous or discontinuous inverted repeats of the nGAAn unit (Enoki and Sakurai, 2011), subsequently resulting in the transcription of heat shock protein genes and other heat-inducible genes (Nover et al, 2001;von Koskull-Döring et al, 2007).…”

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confidence: 99%

An Autoregulatory Loop Controlling Arabidopsis HsfA2 Expression: Role of Heat Shock-Induced Alternative Splicing

et al. 2013

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Heat shock transcription factorA2 (HsfA2) is a key regulator in response to heat stress in Arabidopsis (Arabidopsis thaliana), and its heat shock (HS)-induced transcription regulation has been extensively studied. Recently, alternative splicing, a critical posttranscriptional event, has been shown to regulate HS-inducible expression of HsfA2; however, the molecular mechanism remains largely unknown. Here, we demonstrate a new heat stress-induced splice variant, HsfA2-III, is involved in the self-regulation of HsfA2 transcription in Arabidopsis. HsfA2-III is generated through a cryptic 59 splice site in the intron, which is activated by severe heat (42°C-45°C). We confirmed that HsfA2-III encodes a small truncated HsfA2 isoform (S-HsfA2) by an immunoblot assay with anti-S-HsfA2 antiserum. S-HsfA2 has an extra leucine-rich motif next to its carboxyl-terminal truncated DNA-binding domain. The biological significance of S-HsfA2 was further demonstrated by its nuclear localization and heat shock element (HSE)-binding ability. In yeast (Saccharomyces cerevisiae), the leucine-rich motif can inhibit the transcriptional activation activity of S-HsfA2, while it appears not to be required for the truncated DNA-binding domain-mediated binding ability of S-HsfA2-HSE. Further results reveal that S-HsfA2 could bind to the TATA box-proximal clusters of HSE in the HsfA2 promoter to activate its own transcription. This S-HsfA2-modulated HsfA2 transcription is not mediated through homodimer or heterodimer formation with HsfA1d or HsfA1e, which are known transcriptional activators of HsfA2. Altogether, our findings provide new insights into how HS posttranscriptionally regulates HsfA2 expression. Severe HS-induced alternative splicing also occurs in four other HS-inducible Arabidopsis Hsf genes, suggesting that it is a common feature among Arabidopsis Hsfs.

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Diversity in DNA recognition by heat shock transcription factors (HSFs) from model organisms

Cited by 20 publications

References 23 publications

Accurate Prediction of Inducible Transcription Factor Binding Intensities In Vivo

Accurate Prediction of Inducible Transcription Factor Binding Intensities In Vivo

Distinct heat shock factors and chromatin modifications mediate the organ‐autonomous transcriptional memory of heat stress

An Autoregulatory Loop Controlling Arabidopsis HsfA2 Expression: Role of Heat Shock-Induced Alternative Splicing

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