scholarly journals Large-scale comparative transcriptomic analysis of temperature-responsive genes in Arabidopsis thaliana

Author(s):  
Napaporn Sriden ◽  
Varodom Charoensawan

Abstract Key message Comparative transcriptomic analysis provides broad and detailed understandings of transcriptional responses to a wide range of temperatures in different plant tissues, and unique regulatory functions of temperature-mediating transcription factors. Abstract Climate change poses a great threat to plant diversity and food security. It is thus of necessity to understand the molecular mechanisms for perceiving and responding to adverse temperature changes, to develop the cultivars that are resilient to these environmental stresses. Making use of publicly available datasets, we gathered and re-analyzed 259 individual transcriptomic profiles from 139 unique experiments of Arabidopsis thaliana’s shoot, root, and seedling tissues, subjected to a wide variety of temperature conditions, ranging from freezing, cold, low and high ambient temperatures, to heat shock. Despite the underlying differences in the overall transcriptomic profiles between the plant tissues, we were able to identify distinct sets of genes whose transcription patterns were highly responsive to different types of temperature conditions, some were common among the tissues and some were tissue-specific. Interestingly, we observed that the known temperature-responsive genes such as the heat-shock factor (HSF) family, were up-regulated not only in response to high temperatures, but some of its members were also likely involved in the cold response. By integrating the DNA-binding specificity information of the key temperature transcription factor (TF) HSFA1a, PIF4, and CBFs, we elucidated their distinct DNA-binding patterns to the target genes that showed different transcriptional responses. Taken together, we have comprehensively characterized the transcription patterns of temperature-responsive genes and provided directly testable hypotheses on the regulatory roles of key temperature TFs on the expression dynamics of their target genes.

Author(s):  
Qianglai Tan ◽  
Zhen Zeng ◽  
Feng Xu ◽  
Hua Wei

With the ability to cross placental barriers in their hosts, strains of Gram-positive Enterococcus faecalis can exhibit either beneficial or harmful properties. However, the mechanisms underlying these effects have yet to be determined. A comparative transcriptomic analysis of human placental trophoblasts in response to pathogenic or probiotic E. faecalis was performed in order to investigate the molecular basis of different traits. Results indicated that both E. faecalis Symbioflor 1 and V583 could pass through the placental barrier in vitro with similar levels of invasion ability. In total, 2353 (1369 upregulated and 984 downregulated) and 2351 (1233 upregulated and 1118 downregulated) DEGs were identified in Symbioflor 1 and V583, respectively. Furthermore, 1074 (671 upregulated and 403 downregulated) and 1072 (535 upregulated and 537 downregulated) DEGs were only identified in Symbioflor 1 and V583 treatment groups, respectively. KEGG analysis showed that 6 and 9 signaling pathways were associated with interactions between Symbioflor 1 and V583. GO analysis revealed that these DEGs were mainly related to cellular and metabolic processes and biological regulation. However, 28 and 44 DEGs were classified into terms associated with placental and embryonic development in Symbioflor 1 and V583 treatment groups, respectively. Notably, 9 and 25 unique DEGs were identified only in Symbioflor 1 and V583 treatment groups, respectively. A large proportion of transcriptional responses differed when compared between pathogenic and probiotic E. faecalis interaction, and several unique DEGs and signal pathways were identified in the two different groups. These data enhance our understanding of how different traits can be affected by pathogenic and probiotic E. faecalis and the mechanisms underlying these effects.


2015 ◽  
Vol 4 (5) ◽  
pp. 51 ◽  
Author(s):  
Sujata A. Sirsat ◽  
Christopher A. Baker ◽  
Si Hong Park ◽  
Arunachalam Muthaiyan ◽  
Scot E. Dowd ◽  
...  

<em>Salmonella enterica</em> has been associated with a variety of food products, and thermal treatments are commonly used to reduce or eliminate pathogens from these foods. While the physiological response of <em>Salmonella</em> to a wide range of lethal and sublethal heating temperatures has been examined, only limited information is available at the transcriptional level. The objective of this study was to investigate the transcriptional profile of <em>Salmonella</em> Typhimurium when subjected to thermal shock at 48 °C (10 min). Transcriptomic analysis was performed using partial microarrays (1152 genes) consisting of quorum sensing, virulence, membrane, and stress related genes. Apparent <em>Salmonella</em> viability based on the optical density decreased in response to thermal exposure. Transcriptomic analysis revealed induction of several heat shock and stress related genes due to thermal exposure at 48 °C. This research reveals that there is an impact of exposure to a sublethal temperature (48°C) on the subsequent transcriptional responses of <em>S.</em> Typhimurium.


2019 ◽  
Author(s):  
Christopher M. Uyehara ◽  
Daniel J. McKay

ABSTRACTThe ecdysone pathway was amongst the first experimental systems employed to study the impact of steroid hormones on the genome. In Drosophila and other insects, ecdysone coordinates developmental transitions, including wholesale transformation of the larva into the adult during metamorphosis. Like other hormones, ecdysone controls gene expression through a nuclear receptor, which functions as a ligand-dependent transcription factor. Although it is clear that ecdysone elicits distinct transcriptional responses within its different target tissues, the role of its receptor, EcR, in regulating target gene expression is incompletely understood. In particular, EcR initiates a cascade of transcription factor expression in response to ecdysone, making it unclear which ecdysone-responsive genes are direct EcR targets. Here, we use the larval-to-prepupal transition of developing wings to examine the role of EcR in gene regulation. Genome-wide DNA binding profiles reveal that EcR exhibits widespread binding across the genome, including at many canonical ecdysone-response genes. However, the majority of its binding sites reside at genes with wing-specific functions. We also find that EcR binding is temporally dynamic, with thousands of binding sites changing over time. RNA-seq reveals that EcR acts as both a temporal gate to block precocious entry to the next developmental stage as well as a temporal trigger to promote the subsequent program. Finally, transgenic reporter analysis indicates that EcR regulates not only temporal changes in target enhancer activity but also spatial patterns. Together, these studies define EcR as a multipurpose, direct regulator of gene expression, greatly expanding its role in coordinating developmental transitions.SIGNIFICANCENuclear receptors (NRs) are sequence-specific DNA binding proteins that act as intracellular receptors for small molecules such as hormones. Prior work has shown that NRs function as ligand-dependent switches that initiate a cascade of gene expression changes. The extent to which NRs function as direct regulators of downstream genes in these hierarchies remains incompletely understood. Here, we study the role of the NR EcR in metamorphosis of the Drosophila wing. We find that EcR directly regulates many genes at the top of the hierarchy as well as at downstream genes. Further, we find that EcR binds distinct sets of target genes at different developmental times. This work helps inform how hormones elicit tissue- and temporal-specific responses in target tissues.


2020 ◽  
Author(s):  
Clément Immarigeon ◽  
Sandra Bernat-Fabre ◽  
Emmanuelle Guillou ◽  
Alexis Verger ◽  
Elodie Prince ◽  
...  

AbstractThe evolutionarily-conserved multiprotein Mediator complex (MED) serves as an interface between DNA-bound transcription factors (TFs) and the RNA Polymerase II machinery. It has been proposed that each TF interacts with a dedicated MED subunit to induce specific transcriptional responses. However, binary MED subunit - TF partnerships are probably oversimplified models. Using Drosophila TFs of the GATA family - Pannier (Pnr) and Serpent (Srp) - as a model, we have previously established GATA cofactor evolutionarily-conserved function for the Med1 Mediator subunit. Here, we show that another subunit, Med19, is required for GATA-dependent gene expression and interacts physically with Pnr and Srp in cellulo, in vivo and in vitro through their conserved C-zinc finger (ZF), indicating general GATA co-activator functions. Interestingly, Med19 is critical for the regulation of all tested GATA target genes which is not the case for Med1, suggesting differential use of MED subunits by GATAs depending on the target gene. Lastly, despite their presumed distant position within the MED middle module, both subunits interact physically. In conclusion, our data shed new light first on the MED complex, engaging several subunits to mediate TF-driven transcriptional responses and second, on GATA TFs, showing that ZF DNA-binding domain also serves for transactivation.


1996 ◽  
Vol 16 (1) ◽  
pp. 219-227 ◽  
Author(s):  
F X Claret ◽  
T Antakly ◽  
M Karin ◽  
F Saatcioglu

Thyroid hormone (T3) receptors (T3Rs) are ligand-modulated transcription factors that bind to thyroid hormone response elements (T3REs) and mediate either positive or negative transcriptional regulation of target genes. In addition, in response to ligand binding, T3Rs can interfere with AP-1 activity and thereby inhibit transcription of AP-1-responsive genes. T3Rs were recently shown to form heterodimers with retinoid X receptors (RXRs), leading to increased binding to T3REs in vitro and potentiation of transcriptional responses in vivo. Here we demonstrate that T3R alpha forms stable heterodimers with RXR alpha in living cells. Most important, we describe a new role for RXR alpha in modulating ligand-dependent T3R alpha activity: heterodimerization with RXR alpha greatly increases transcriptional interference with AP-1 activity, augments T3-dependent transcriptional activation, and potentiates the reversal of ligand-independent activation by T3R alpha. In all three cases, the responses occur at substantially lower T3 concentrations when elicited by T3R alpha plus RXR alpha than by T3R alpha alone. In vitro, the binding of T3 decreases the DNA-binding activity of T3R alpha homodimers but does not affect DNA binding by T3R alpha:RXR alpha heterodimers. We provide evidence that increased activities of T3R alpha at lower T3 concentrations are not due to changes in its T3 binding properties. Instead, the altered response could be mediated by either RXR alpha-induced conformational changes, increased stability of heterodimers over homodimers, especially following T3 binding, or both.


Authorea ◽  
2020 ◽  
Author(s):  
Xiao Wang ◽  
Binzhong Wang ◽  
Kailu Chen ◽  
Zhonghuan Tian ◽  
Chaoan Long ◽  
...  

BMC Genomics ◽  
2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Alwyn C. Go ◽  
Alberto Civetta

Abstract Background The genetic basis of hybrid incompatibilities is characterized by pervasive cases of gene interactions. Sex chromosomes play a major role in speciation and X-linked hybrid male sterility (HMS) genes have been identified. Interestingly, some of these genes code for proteins with DNA binding domains, suggesting a capability to act as trans-regulatory elements and disturb the expression of a large number of gene targets. To understand how interactions between trans- and cis-regulatory elements contribute to speciation, we aimed to map putative X-linked trans-regulatory elements and to identify gene targets with disrupted gene expression in sterile hybrids between the subspecies Drosophila pseudoobscura pseudoobscura and D. p. bogotana. Results We find six putative trans-regulatory proteins within previously mapped X chromosome HMS loci with sequence changes that differentiate the two subspecies. Among them, the previously characterized HMS gene Overdrive (Ovd) had the largest number of amino acid changes between subspecies, with some substitutions localized within the protein’s DNA binding domain. Using an introgression approach, we detected transcriptional responses associated with a sterility/fertility Ovd allele swap. We found a network of 52 targets of Ovd and identified cis-regulatory effects among target genes with disrupted expression in sterile hybrids. However, a combined analysis of polymorphism and divergence in non-coding sequences immediately upstream of target genes found no evidence of changes in candidate regulatory proximal cis-elements. Finally, peptidases were over-represented among target genes. Conclusions We provide evidence of divergence between subspecies within the DNA binding domain of the HMS protein Ovd and identify trans effects on the expression of 52 gene targets. Our results identify a network of trans-cis interactions with possible effects on HMS. This network provides molecular evidence of gene × gene incompatibilities as contributors to hybrid dysfunction.


2006 ◽  
Vol 26 (9) ◽  
pp. 3514-3526 ◽  
Author(s):  
Cheng-Jun Hu ◽  
Sangeeta Iyer ◽  
Aneesa Sataur ◽  
Kelly L. Covello ◽  
Lewis A. Chodosh ◽  
...  

ABSTRACT Transcriptional responses to hypoxia are primarily mediated by hypoxia-inducible factors (HIFs), HIF-1α and HIF-2α. The HIF-1α and HIF-2α subunits are structurally similar in their DNA binding and dimerization domains but differ in their transactivation domains, implying they may have unique target genes and require distinct transcriptional cofactors. Our previous results demonstrated that HIF-1α and HIF-2α regulate distinct target genes. Here, we report that HIF-2α is not transcriptionally active in embryonic stem (ES) cells, as well as possible inhibition by a HIF-2α-specific transcriptional repressor. Using DNA microarray analysis of hypoxia-inducible genes in wild-type (WT), Hif-1α − / − , and Hif-2α − / − ES cells, we show that HIF-1α induces a large number of both confirmed and novel hypoxia-inducible genes, while HIF-2α does not activate any of its previously described targets. We further demonstrate that inhibition of HIF-2α function occurs at the level of transcription cofactor recruitment to endogenous target gene promoters. Overexpression of WT and, notably, a DNA-binding-defective HIF-2α mutant restores endogenous HIF-2α protein activity, suggesting that ES cells express a HIF-2α-specific corepressor that can be titrated by overexpressed HIF-2α protein. HIF-2α repression may explain why patients with mutations in the VHL tumor suppressor gene display cancerous lesions in specific tissue types.


Sign in / Sign up

Export Citation Format

Share Document