Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA221720 | ENA |
REPOSITORIES: ENA
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Project description:Multiple transcription factors (TFs) play essential roles in plants under abiotic stress, one of the most challenging conditions of plant survival. However, how these multiple TFs cooperate in abiotic stress responses still remains largely unknown. In this study, we provide evidence that a novel NAC (NAM, ATAF1/2, and CUC2) transcription factor (ANAC096) cooperates with bZIP-type TFs [ABRE-binding factor/ABRE-binding protein (ABF/AREB)] in ensuring survival under dehydration and osmotic stress conditions. Intriguingly, ANAC096 directly interacted with ABF2 and ABF4, but not with ABF3, both in vitro and in vivo. ANAC096 and ABF2 synergistically activated RD29A transcription. The genome-wide gene expression analysis revealed that a major proportion of ABA-responsive genes are under the transcriptional regulation of ANAC096.An Arabidopsis mutant, anac096, was hyposensitive to exogenous abscisic acid (ABA), and showed impaired ABA-induced stomatal closure and increased water loss under dehydration stress conditions. Furthermore, the anac096 abf2 abf4 triple mutant was much more sensitive to dehydration and osmotic stresses than the anac096 single mutant or the abf2 abf4 double-mutant. Based on these results, we propose that ANAC096 is involved in a synergistic relationship with a subset of ABFs for the transcriptional activation of ABA-inducible genes in response to dehydration and osmotic stresses.
2014-01-02 | GSE51218 | GEO
Project description:Multiple transcription factors (TFs) play essential roles in plants under abiotic stress, one of the most challenging conditions of plant survival. However, how these multiple TFs cooperate in abiotic stress responses still remains largely unknown. In this study, we provide evidence that a novel NAC (NAM, ATAF1/2, and CUC2) transcription factor (ANAC096) cooperates with bZIP-type TFs [ABRE-binding factor/ABRE-binding protein (ABF/AREB)] in ensuring survival under dehydration and osmotic stress conditions. Intriguingly, ANAC096 directly interacted with ABF2 and ABF4, but not with ABF3, both in vitro and in vivo. ANAC096 and ABF2 synergistically activated RD29A transcription. The genome-wide gene expression analysis revealed that a major proportion of ABA-responsive genes are under the transcriptional regulation of ANAC096.An Arabidopsis mutant, anac096, was hyposensitive to exogenous abscisic acid (ABA), and showed impaired ABA-induced stomatal closure and increased water loss under dehydration stress conditions. Furthermore, the anac096 abf2 abf4 triple mutant was much more sensitive to dehydration and osmotic stresses than the anac096 single mutant or the abf2 abf4 double-mutant. Based on these results, we propose that ANAC096 is involved in a synergistic relationship with a subset of ABFs for the transcriptional activation of ABA-inducible genes in response to dehydration and osmotic stresses. pTA plants (12-day-old) cultured in liquid medium were treated with 30 uM Dex alone for 1 h (Control) or 30 uM Dex alone for 30 min followed by an additional treatment of 30 min with both 30 uM Dex and 2 uM ABA (ABA). For pTA-ANAC096 plants, 12-day-old seedlings were treated with 30 uM Dex for 1 h (ANAC096) or with 30 uM Dex only for 0.5 h followed by additional 0.5 h incubation with both 2 uM ABA and 30 uM Dex (ANAC096+ABA). Total RNAs were isolated from two biological replicates at each condition and used to measure gene expression level.
2014-01-02 | E-GEOD-51218 | biostudies-arrayexpress
Project description:Despite the potential of the endoplasmic reticulum (ER) stress response to accommodate adaptive pathways, its integration with other environmental-induced responses is poorly understood in plants. Here, we performed global expression profiling on soybean leaves exposed to polyethylene glycol treatment or to unfolded protein response (UPR) inducers to identify integrated networks between osmotic and ER stress-induced adaptive responses. The results unmasked the major branches of the ER-stress response, which includes enhancing protein folding and degradation in the ER, as well as specific osmotically regulated changes linked to cellular responses induced by dehydration. However, a small proportion (5.5%) of total up-regulated genes represented a shared response that seemed to integrate the two signaling pathways. These co-regulated genes were considered downstream targets based on similar induction kinetics and a synergistic response to the combination of osmotic- and ER-stress-inducing treatments. Genes in this integrated pathway with the strongest synergistic induction encoded proteins with diverse roles. Two of them contained a plant-specific development and cell death (DCD) domain while another had homology to proteins with an ubiquitin-associated (UBA) domain. A NAC domain-containing protein exhibited robust early kinetics of induction consistent with a role as a transfactor. This integrated pathway diverged further from characterized ER-specific branches of UPR as downstream targets were inversely regulated by osmotic stress. Collectively, our results describe a novel branch of the ER stress response that integrates the osmotic signal to potentiate transcription of shared target genes. Keywords: stress response
2007-09-12 | GSE8992 | GEO
Project description:During late- and post-ripening stages, grape berry undergoes profound biochemical and physiological changes whose molecular control is poorly understood. Here, we report the role of NAC61, a grapevine NAC transcription factor, in regulating different processes featuring the berry ripening progression. NAC61 is highly expressed during post-harvest berry dehydration and its expression pattern is closely related to sugar concentration. The ectopic expression of NAC61 in Nicotiana benthamiana leaves determines low stomatal conductance, high leaf temperature, tissue collapse and a higher relative water content. Transcriptome analysis of grapevine leaves transiently overexpressing NAC61, and DNA affinity purification and sequencing analyses allowed us to narrow down a list of NAC61-regulated genes. Direct regulation of the stilbene synthase regulator MYB14, the osmotic stress-related gene DHN1b, the Botrytis cinerea susceptibility gene WRKY52 and the NAC61 itself, is validated. We also demonstrate that NAC61 interacts with NAC60, a proposed master regulator of grapevine organ maturation, in the activation of MYB14 and NAC61 expression. Overall, our findings establish NAC61 as a key player in a regulative network that governs stilbenoid metabolism and osmotic, oxidative and biotic stress responses that hallmark late- and post-ripening grape stages.
2024-01-25 | GSE232165 | GEO
Project description:Skeletal muscle atrophy is a highly prevalent and debilitating condition that remains poorly understood at the molecular level. Previous work found that skeletal muscle atrophy involves activating transcription factor 4 (ATF4), a protein in the basic leucine zipper (bZIP) transcription factor family. However, the direct biochemical mechanism by which ATF4 promotes muscle atrophy was unknown. Because bZIP proteins such as ATF4 must dimerize to bind and activate genes, and because ATF4 is unable to form highly stable homodimers, we hypothesized that ATF4 may promote muscle atrophy by heterodimerizing with another bZIP family member. To test this hypothesis, we biochemically isolated skeletal muscle proteins that associate with the dimerization- and DNA-binding domain of ATF4 (the bZIP domain) in mouse skeletal muscle fibers in vivo. Interestingly, we found that ATF4 makes up one half of at least 5 distinct heterodimeric bZIP transcription factors in skeletal muscle fibers. This three-way interaction between ATF4, C/EBPbeta and the ATF4-C/EBP composite site activates the Gadd45a gene, which encodes a known mediator of muscle atrophy (Gadd45a). Together, these results identify a direct biochemical mechanism by which ATF4 induces skeletal muscle atrophy and provide new insight into the way that skeletal muscle atrophy occurs at the molecular level.
2019-11-04 | MSV000084538 | MassIVE
Project description:The epidermal barrier protects the body against mechanical injury, infection and dehydration. The respective contribution of type I and type II keratins which form the major cytoskeleton in epidermal keratinocytes in barrier formation and stress protection is incompletely understood. Here, we reveal a novel mechanism by which keratins control anti-oxidant responses through barrier-dependent and cell-autonomous mechanisms. Mice lacking the entire type I (KtyI) or type II (KtyII) keratin gene clusters suffer from distinct prenatal barrier defects. Comparative transcriptome profiling identifies essential cornified envelope components and reveals strong upregulation of the bZIP transcription factor Nrf2 in situ. Isolated keratinocytes from both strains of mice show elevated mitochondrial oxygen consumption and Nrf2 activity, decreased upon keratin re-expression. We propose a model in which keratins control mitochondria-derived oxidative stress via Nrf2 activation. Our findings reveal major contributions of keratins to chronic inflammation and autoimmune disorders. Total RNA obtained from E18.5 embryo back skin from typeI and II keratin knockout compared with respective wild type.
2016-03-26 | E-GEOD-79590 | biostudies-arrayexpress
Project description:Repeated exposure to cocaine causes sensitized behavioral responses and increased dendritic spines on medium spiny neurons of the nucleus accumbens (NAc). We find that cocaine regulates myocyte enhancer factor 2 (MEF2) transcription factors to control these two processes in vivo. Cocaine suppresses striatal MEF2 activity in part through a novel mechanism involving cAMP, the regulator of calmodulin signaling (RCS), and calcineurin. We show that reducing MEF2 activity in the NAc in vivo is required for the cocaine-induced increases in dendritic spine density. Surprisingly, we find that increasing MEF2 activity in the NAc, which blocks the cocaine-induced increase in dendritic spine density, enhances sensitized behavioral responses to cocaine. Together, our findings implicate MEF2 as a key regulator of structural synapse plasticity and sensitized responses to cocaine, and suggest that reducing MEF2 activity (and increasing spine density) in NAc may be a compensatory mechanism to limit long-lasting maladaptive behavioral responses to cocaine.
2008-08-24 | GSE11939 | GEO
Project description:Distinct and essential role of bZIP transcription factors as regulators of stress responses
| PRJNA656145 | ENA
Project description:In order to dissect the gene regulatory network during the functional transition of cotyledons from non-photosynthetic storage tissue to metabolically active photosynthetic tissue, we constructed ChIP-Seq libraries for NAC and YABBY transcription factors using pooled cotyledons from seedling developmental stage 4 and stage 5. Millions of raw reads obtained from ChIP-Seq libraries were aligned to the reference soybean genome using the ultrafast Bowtie aligner to obtain quantitative data for genome matched reads. MACS software was used to call peaks representing enriched binding sites for NAC and YABBY transcription factors. Based on our ChIP-Seq data, we identified 72 genes are potentially regulated by NAC transcription factor and 96 genes by YABBY transcription factor. The motif analysis using MEME discovered three separate motifs for the NAC and YABBY transcription factors. For the NAC transcription factor, three commonly found motifs were G[AT]G[AG]G[AG]GA, C[AC]C[GA][TC][GA]CC and TGGGCC . The first one matched to a known zinc finger motif and the last two were identified as leucine zippers in the database of plant transcription factor binding motifs, JASPAR CORE plants. Similarly the three most commonly found motifs for YABBY transcription factors are CC [CA][TC]C[TA][CT]C, GA[AG]AGAAA and CCCCAC . The first two motifs matched to a known zinc finger motif and the last one was an AP2 MBD-like motif. Construction of ChIP-Seq libraries for NAC and YABBY transcription factors using germinating cotyledons from seedling developmental stages
2013-08-14 | E-GEOD-42422 | biostudies-arrayexpress
Project description:The epidermal barrier protects the body against mechanical injury, infection and dehydration. The respective contribution of type I and type II keratins which form the major cytoskeleton in epidermal keratinocytes in barrier formation and stress protection is incompletely understood. Here, we reveal a novel mechanism by which keratins control anti-oxidant responses through barrier-dependent and cell-autonomous mechanisms. Mice lacking the entire type I (KtyI) or type II (KtyII) keratin gene clusters suffer from distinct prenatal barrier defects. Comparative transcriptome profiling identifies essential cornified envelope components and reveals strong upregulation of the bZIP transcription factor Nrf2 in situ. Isolated keratinocytes from both strains of mice show elevated mitochondrial oxygen consumption and Nrf2 activity, decreased upon keratin re-expression. We propose a model in which keratins control mitochondria-derived oxidative stress via Nrf2 activation. Our findings reveal major contributions of keratins to chronic inflammation and autoimmune disorders.
2016-03-26 | GSE79590 | GEO