scholarly journals Transcriptional regulation of KCS gene by bZIP29 and MYB70 transcription factors during ABA-stimulated wound suberization of kiwifruit (Actinidia deliciosa)

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Xueyuan Han ◽  
Xiaopeng Wei ◽  
Wenjing Lu ◽  
Qiong Wu ◽  
Linchun Mao ◽  
...  

Abstract Background Our previous study has demonstrated that the transcription of AchnKCS involved in suberin biosynthesis was up-regulated by exogenous abscisic acid (ABA) during the wound suberization of kiwifruit, but the regulatory mechanism has not been fully elucidated. Results Through subcellular localization analysis in this work, AchnbZIP29 and AchnMYB70 transcription factors were observed to be localized in the nucleus. Yeast one-hybrid and dual-luciferase assay proved the transcriptional activation of AchnMYB70 and transcriptional suppression of AchnbZIP29 on AchnKCS promoter. Furthermore, the transcription level of AchnMYB70 was enhanced by ABA during wound suberization of kiwifruit, but AchnbZIP29 transcription was reduced by ABA. Conclusions Therefore, it was believed that ABA enhanced the transcriptional activation of AchnMYB70 on AchnKCS by increasing AchnMYB70 expression. On the contrary, ABA relieved the inhibitory effect of AchnbZIP29 on transcription of AchnKCS by inhibiting AchnbZIP29 expression. These results gave further insight into the molecular regulatory network of ABA in wound suberization of kiwifruit.

2021 ◽  
Author(s):  
Xueyuan Han ◽  
Xiaopeng Wei ◽  
Wenjing Lu ◽  
Qiong Wu ◽  
Linchun Mao

Abstract Background: Our previous study has demonstrated that the transcription of AchnKCS involved in suberin biosynthesis was up-regulated by exogenous abscisic acid (ABA) during the wound suberization of kiwifruit, but the regulatory mechanism has not been fully elucidated. Results: Through subcellular localization analysis in this work, AchnbZIP29 and AchnMYB70 transcription factors were observed to be localized in the nucleus. Yeast one-hybrid and dual-luciferase assay proved the transcriptional activation of AchnMYB70 and transcriptional suppression of AchnbZIP29 on AchnKCS promoter. Furthermore, the transcription level of AchnMYB70 was enhanced by ABA during wound suberization of kiwifruit, but AchnbZIP29 transcription was reduced by ABA.Conclusions: Therefore, it was believed that ABA enhanced the transcriptional activation of AchnMYB70 on AchnKCS by increasing AchnMYB70 expression. On the contrary, ABA relieved the inhibitory effect of AchnbZIP29 on transcription of AchnKCS by inhibiting AchnbZIP29 expression. These results gave further insight into the molecular regulatory network of ABA in wound suberization of kiwifruit.


Gut ◽  
2019 ◽  
Vol 69 (4) ◽  
pp. 630-640 ◽  
Author(s):  
Li Chen ◽  
Moli Huang ◽  
Jasmine Plummer ◽  
Jian Pan ◽  
Yan Yi Jiang ◽  
...  

ObjectiveWhile oesophageal squamous cell carcinoma remains infrequent in Western populations, the incidence of oesophageal adenocarcinoma (EAC) has increased sixfold to eightfold over the past four decades. We aimed to characterise oesophageal cancer-specific and subtypes-specific gene regulation patterns and their upstream transcription factors (TFs). DesignTo identify regulatory elements, we profiled fresh-frozen oesophageal normal samples, tumours and cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematical modelling was performed to establish (super)-enhancers landscapes and interconnected transcriptional circuitry formed by master TFs. Coregulation and cooperation between master TFs were investigated by ChIP-Seq, circularised chromosome conformation capture sequencing and luciferase assay. Biological functions of candidate factors were evaluated both in vitro and in vivo.ResultsWe found widespread and pervasive alterations of the (super)-enhancer reservoir in both subtypes of oesophageal cancer, leading to transcriptional activation of a myriad of novel oncogenes and signalling pathways, some of which may be exploited pharmacologically (eg, leukemia inhibitory factor (LIF) pathway). Focusing on EAC, we bioinformatically reconstructed and functionally validated an interconnected circuitry formed by four master TFs—ELF3, KLF5, GATA6 and EHF—which promoted each other’s expression by interacting with each super-enhancer. Downstream, these master TFs occupied almost all EAC super-enhancers and cooperatively orchestrated EAC transcriptome. Each TF within the transcriptional circuitry was highly and specifically expressed in EAC and functionally promoted EAC cell proliferation and survival.ConclusionsBy establishing cancer-specific and subtype-specific features of the EAC epigenome, our findings promise to transform understanding of the transcriptional dysregulation and addiction of EAC, while providing molecular clues to develop novel therapeutic modalities against this malignancy.


2006 ◽  
Vol 27 (2) ◽  
pp. 579-594 ◽  
Author(s):  
Stephanie Roessler ◽  
Ildiko Györy ◽  
Sascha Imhof ◽  
Mikhail Spivakov ◽  
Ruth R. Williams ◽  
...  

ABSTRACT Early differentiation of B lymphocytes requires the function of multiple transcription factors that regulate the specification and commitment of the lineage. Loss- and gain-of-function experiments have provided important insight into the transcriptional control of B lymphopoiesis, whereby E2A was suggested to act upstream of EBF1 and Pax5 downstream of EBF1. However, this simple hierarchy cannot account for all observations, and our understanding of a presumed regulatory network, in which transcription factors and signaling pathways operate, is limited. Here, we show that the expression of the Ebf1 gene involves two promoters that are differentially regulated and generate distinct protein isoforms. We find that interleukin-7 signaling, E2A, and EBF1 activate the distal Ebf1 promoter, whereas Pax5, together with Ets1 and Pu.1, regulates the stronger proximal promoter. In the absence of Pax5, the function of the proximal Ebf1 promoter and accumulation of EBF1 protein are impaired and the replication timing and subcellular localization of the Ebf1 locus are altered. Taken together, these data suggest that the regulation of Ebf1 via distinct promoters allows for the generation of several feedback loops and the coordination of multiple determinants of B lymphopoiesis in a regulatory network.


2021 ◽  
Author(s):  
Xiaoxue Fang ◽  
Manqi Wang ◽  
Xinteng Zhou ◽  
Huan Wang ◽  
Huaying Wang ◽  
...  

Abstract Background: As a famous Chinese medicine, ginseng has been used in the world for nearly 5,000 years. Wild ginseng is endangered due to environmental damage. Thus, cultivated ginseng is developed to replace wild ginseng. The morphological and physiological characteristics of both wild ginseng and cultivated ginseng change during growth, and the mechanism of this change is not yet understood. Results: This study performed transcriptome sequencing on the roots, stems and leaves of cultivated ginseng and wild ginseng with different growth years, exploring the effect of growth years on gene expression in ginseng. The number of DEGs in cultivated ginseng is more than that in wild ginseng. Based on the weighted gene co-expression network analysis, we found that the growth years significantly affected the gene expression of MAPK signaling pathway - plant and terpenoid backbone biosynthesis pathway in cultivated ginseng, but had no effects in wild ginseng. Furthermore, the growth years had significant effects on the genes related to ginsenoside synthesis in cultivated ginseng, and the effects were different in the roots, stems and leaves. However, it had little influence on the expression of genes related to ginsenoside synthesis in wild ginseng and no effect on leaves. These results showed wild ginseng was less affected by growth years than cultivated ginseng. Furthermore, HMGR, SS, DXS, DS, IspF, AACT, CYP450 and UGTs were related with MYB, NAC, AP2/ERF, bHLH and WRKY transcription factors. Growth years may regulate genes for ginsenoside synthesis by influencing these transcription factors, thereby affecting the content of ginsenosides.Conclusions: This study complemented the gaps in the genetic information of wild ginseng in different growth periods and different tissues and provided a new insight into the mechanism of ginsenoside regulation.


2020 ◽  
Author(s):  
Jinliang Yue ◽  
Shu-feng Zheng

Abstract Background: The haplotype in MALAT1 affects its expression and is correlated with human diseases like Normal Tension Glaucoma (NTG), although its detailed mechanism remains unclear. Methods: Quantitative real-time PCR was performed to assess the expression of MALAT1, miR-1 and IL-6 in the serum of NTG patients with different haplotypes of MALAT1, as well as in HUVEC and HTMC cells transfected with MALAT1. ELISA was used to analyze the IL-6 level in the serum of NTG patients. RNFL thickness, RA and C/D ratio were calculated for NTG patients. A luciferase assays was carried out to evaluate the inhibitory effect of miR-1 on MALAT1 and IL-6 expression. Western blot was used to analyze the IL-6 protein level in HUVEC and HTMC cells transfected with MALAT1.Results: Accordingly, GGGT haplotype was demonstrated to be associated with a decreased risk of NTG. The MALAT1 level in serum of NTG patients carrying GGGT haplotype was significantly decreased compared with NTG patients carrying other haplotypes, along with elevated miR-1 expression and diminished IL-6 expression. NTG patients carrying GGGT haplotype had thicker RNFL and RA, but a smaller C/D ratio. Sequence analysis found potential target sites of miR-1 on MALAT1 and IL-6, and luciferase assay confirmed the inhibitory effect of miR-1 on MALAT1 and IL-6 expression. Meanwhile, MALAT1 also down-regulated miR-1 expression and consequently up-regulated IL-6 expression. Conclusion: This study presented evidence for a regulatory network containing MALAT1, miR-1 and IL-6, and further demonstrated the effect of MALAT1 haplotype on the risk and severity of NTG.


2022 ◽  
Author(s):  
Xiaoxue Fang ◽  
Manqi Wang ◽  
Xinteng Zhou ◽  
Huan Wang ◽  
Huaying Wang ◽  
...  

Abstract Background: As a famous Chinese medicine, ginseng has been used in the world for nearly 5,000 years. Wild ginseng is endangered due to environmental damage. Thus, cultivated ginseng is developed to replace wild ginseng. The morphological and physiological characteristics of both wild ginseng and cultivated ginseng change during growth, and the mechanism of this change is not yet understood. Results: This study performed transcriptome sequencing on the roots, stems and leaves of cultivated ginseng and wild ginseng with different growth years, exploring the effect of growth years on gene expression in ginseng. The number of DEGs in cultivated ginseng is more than that in wild ginseng. Based on the weighted gene co-expression network analysis, we found that the growth years significantly affected the gene expression of MAPK signaling pathway - plant and terpenoid backbone biosynthesis pathway in cultivated ginseng, but had no effects in wild ginseng. Furthermore, the growth years had significant effects on the genes related to ginsenoside synthesis in cultivated ginseng, and the effects were different in the roots, stems and leaves. However, it had little influence on the expression of genes related to ginsenoside synthesis in wild ginseng and no effect on leaves. These results showed wild ginseng was less affected by growth years than cultivated ginseng. Furthermore, HMGR, SS, DXS, DS, IspF, AACT, CYP450 and UGTs were related with MYB, NAC, AP2/ERF, bHLH and WRKY transcription factors. Growth years may regulate genes for ginsenoside synthesis by influencing these transcription factors, thereby affecting the content of ginsenosides. Conclusions: This study complemented the gaps in the genetic information of wild ginseng in different growth periods and different tissues and provided a new insight into the mechanism of ginsenoside regulation.


2013 ◽  
Vol 35 (10) ◽  
pp. 1198-1208
Author(s):  
Zhi-Qiang CHEN ◽  
Xin-Huan HAN ◽  
Qin-Jun WEI ◽  
Guang-Qian XING ◽  
Xin CAO

2020 ◽  
Vol 51 (1) ◽  
Author(s):  
Zongyi Bo ◽  
Yurun Miao ◽  
Rui Xi ◽  
Qiuping Zhong ◽  
Chenyi Bao ◽  
...  

Abstract Cyclic GMP-AMP (cGAMP) synthase (cGAS) is an intracellular sensor of cytoplasmic viral DNA created during virus infection, which subsequently activates the stimulator of interferon gene (STING)-dependent type I interferon response to eliminate pathogens. In contrast, viruses have developed different strategies to modulate this signalling pathway. Pseudorabies virus (PRV), an alphaherpesvirus, is the causative agent of Aujeszky’s disease (AD), a notable disease that causes substantial economic loss to the swine industry globally. Previous reports have shown that PRV infection induces cGAS-dependent IFN-β production, conversely hydrolysing cGAMP, a second messenger synthesized by cGAS, and attenuates PRV-induced IRF3 activation and IFN-β secretion. However, it is not clear whether PRV open reading frames (ORFs) modulate the cGAS–STING-IRF3 pathway. Here, 50 PRV ORFs were screened, showing that PRV UL13 serine/threonine kinase blocks the cGAS–STING-IRF3-, poly(I:C)- or VSV-mediated transcriptional activation of the IFN-β gene. Importantly, it was discovered that UL13 phosphorylates IRF3, and its kinase activity is indispensable for such an inhibitory effect. Moreover, UL13 does not affect IRF3 dimerization, nuclear translocation or association with CREB-binding protein (CBP) but attenuates the binding of IRF3 to the IRF3-responsive promoter. Consistent with this, it was discovered that UL13 inhibits the expression of multiple interferon-stimulated genes (ISGs) induced by cGAS–STING or poly(I:C). Finally, it was determined that PRV infection can activate IRF3 by recruiting it to the nucleus, and PRVΔUL13 mutants enhance the transactivation level of the IFN-β gene. Taken together, the data from the present study demonstrated that PRV UL13 inhibits cGAS–STING-mediated IFN-β production by phosphorylating IRF3.


2005 ◽  
Vol 83 (4) ◽  
pp. 535-547 ◽  
Author(s):  
Gareth N Corry ◽  
D Alan Underhill

To date, the majority of the research regarding eukaryotic transcription factors has focused on characterizing their function primarily through in vitro methods. These studies have revealed that transcription factors are essentially modular structures, containing separate regions that participate in such activities as DNA binding, protein–protein interaction, and transcriptional activation or repression. To fully comprehend the behavior of a given transcription factor, however, these domains must be analyzed in the context of the entire protein, and in certain cases the context of a multiprotein complex. Furthermore, it must be appreciated that transcription factors function in the nucleus, where they must contend with a variety of factors, including the nuclear architecture, chromatin domains, chromosome territories, and cell-cycle-associated processes. Recent examinations of transcription factors in the nucleus have clarified the behavior of these proteins in vivo and have increased our understanding of how gene expression is regulated in eukaryotes. Here, we review the current knowledge regarding sequence-specific transcription factor compartmentalization within the nucleus and discuss its impact on the regulation of such processes as activation or repression of gene expression and interaction with coregulatory factors.Key words: transcription, subnuclear localization, chromatin, gene expression, nuclear architecture.


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