scholarly journals A Pathogen-Inducible Rice NAC Transcription Factor ONAC096 Contributes to Immunity Against Magnaprothe oryzae and Xanthomonas oryzae pv. oryzae by Direct Binding to the Promoters of OsRap2.6, OsWRKY62, and OsPAL1

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Wang ◽  
Yan Bi ◽  
Yizhou Gao ◽  
Yuqing Yan ◽  
Xi Yuan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Nac Transcription Factor ◽  
Xanthomonas Oryzae ◽  
Pcr Analysis ◽  
Marker Genes ◽  
Recognition Sequence ◽  
Downstream Target ◽  
Small Set ◽  
Direct Binding

The rice NAC transcriptional factor family harbors 151 members, and some of them play important roles in rice immunity. Here, we report the function and molecular mechanism of a pathogen-inducible NAC transcription factor, ONAC096, in rice immunity against Magnaprothe oryzae and Xanthomonas oryzae pv. oryzae. Expression of ONAC096 was induced by M. oryzae and by abscisic acid and methyl jasmonate. ONAC096 had the DNA binding ability to NAC recognition sequence and was found to be a nucleus-localized transcriptional activator whose activity depended on its C-terminal. CRISPR/Cas9-mediated knockout of ONAC096 attenuated rice immunity against M. oryzae and X. oryzae pv. oryzae as well as suppressed chitin- and flg22-induced reactive oxygen species burst and expression of PTI marker genes OsWRKY45 and OsPAL4; by contrast, overexpression of ONAC096 enhanced rice immunity against these two pathogens and strengthened chitin- or flg22-induced PTI. RNA-seq transcriptomic profiling and qRT-PCR analysis identified a small set of defense and signaling genes that are putatively regulated by ONAC096, and further biochemical analysis validated that ONAC096 could directly bind to the promoters of OsRap2.6, OsWRKY62, and OsPAL1, three known defense and signaling genes that regulate rice immunity. ONAC096 interacts with ONAC066, which is a positive regulator of rice immunity. These results demonstrate that ONAC096 positively contributes to rice immunity against M. oryzae and X. oryzae pv. oryzae through direct binding to the promoters of downstream target genes including OsRap2.6, OsWRKY62, and OsPAL1.

scholarly journals Transcription factor CHF1/Hey2 suppresses cardiac hypertrophy through an inhibitory interaction with GATA4

2006 ◽  
Vol 290 (5) ◽  
pp. H1997-H2006 ◽  
Author(s):  
Fan Xiang ◽  
Yasuhiko Sakata ◽  
Lei Cui ◽  
Joey M. Youngblood ◽  
Hironori Nakagami ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transgenic Mice ◽  
Cardiac Hypertrophy ◽  
Marker Genes ◽  
Recognition Sequence ◽  
Inhibitory Interaction ◽  
Hypertrophic Response ◽  
Neonatal Cardiomyocytes

Pathological cardiac hypertrophy is considered a precursor to clinical heart failure. Understanding the transcriptional regulators that suppress the hypertrophic response may have profound implications for the treatment of heart disease. We report the generation of transgenic mice that overexpress the transcription factor CHF1/Hey2 in the myocardium. In response to the α-adrenergic agonist phenylephrine, they show marked attenuation in the hypertrophic response compared with wild-type controls, even though blood pressure is similar in both groups. Isolated myocytes from transgenic mice demonstrate a similar resistance to phenylephrine-induced hypertrophy in vitro, providing further evidence that the protective effect of CHF1/Hey2 is mediated at the myocyte level. Induction of the hypertrophy marker genes ANF, BNP, and β- MHC in the transgenic cells is concurrently suppressed in vivo and in vitro, demonstrating that the induction of hypertrophy-associated genes is repressed by CHF1/Hey2. Transfection of CHF1/Hey2 into neonatal cardiomyocytes suppresses activation of an ANF reporter plasmid by the transcription factor GATA4, which has previously been shown to activate a hypertrophic transcriptional program. Furthermore, CHF1/Hey2 binds GATA4 directly in coimmunoprecipitation assays and inhibits the binding of GATA4 to its recognition sequence within the ANF promoter. Our findings demonstrate that CHF1/Hey2 functions as an antihypertrophic gene, possibly through inhibition of a GATA4-dependent hypertrophic program.

scholarly journals Distinct Posttranscriptional Mechanisms Regulate the Activity of the Zn Finger Transcription Factor Lame duck during Drosophila Myogenesis

2006 ◽  
Vol 26 (4) ◽  
pp. 1414-1423 ◽  
Author(s):  
Hong Duan ◽  
Hanh T. Nguyen
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Posttranslational Modifications ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Protein Activity ◽  
Downstream Target ◽  
Muscle Formation ◽  
Lame Duck ◽  
Fusion Competent Myoblasts

ABSTRACT Skeletal muscle formation in Drosophila melanogaster requires two types of myoblasts, muscle founders and fusion-competent myoblasts. Lame duck (Lmd), a member of the Gli superfamily of transcription factors, is essential for the specification and differentiation of fusion-competent myoblasts. We report herein that appropriate levels of active Lmd protein are attained by a combination of posttranscriptional mechanisms. We provide evidence that two different regions of the Lmd protein are critical for modulating the balance between its nuclear translocation and its retention within the cytoplasm. Activation of the Lmd protein is also tempered by posttranslational modifications of the protein that do not detectably change its subcellular localization. We further show that overexpression of Lmd protein derivatives that are constitutively nuclear or hyperactive results in severe muscle defects. These findings underscore the importance of regulated Lmd protein activity in maintaining proper activation of downstream target genes, such as Mef2, within fusion-competent myoblasts.

scholarly journals GAGA Regulates Border Cell Migration in Drosophila

2020 ◽  
Vol 21 (20) ◽  
pp. 7468
Author(s):  
Anna A. Ogienko ◽  
Lyubov A. Yarinich ◽  
Elena V. Fedorova ◽  
Natalya V. Dorogova ◽  
Sergey I. Bayborodin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Migration ◽  
Target Genes ◽  
Genetic Interaction ◽  
Follicle Cells ◽  
Collective Cell Migration ◽  
Border Cells ◽  
Drosophila Oogenesis ◽  
Small Set ◽  
Multicellular Organisms

Collective cell migration is a complex process that happens during normal development of many multicellular organisms, as well as during oncological transformations. In Drosophila oogenesis, a small set of follicle cells originally located at the anterior tip of each egg chamber become motile and migrate as a cluster through nurse cells toward the oocyte. These specialized cells are referred to as border cells (BCs) and provide a simple and convenient model system to study collective cell migration. The process is known to be complexly regulated at different levels and the product of the slow border cells (slbo) gene, the C/EBP transcription factor, is one of the key elements in this process. However, little is known about the regulation of slbo expression. On the other hand, the ubiquitously expressed transcription factor GAGA, which is encoded by the Trithorax-like (Trl) gene was previously demonstrated to be important for Drosophila oogenesis. Here, we found that Trl mutations cause substantial defects in BC migration. Partially, these defects are explained by the reduced level of slbo expression in BCs. Additionally, a strong genetic interaction between Trl and slbo mutants, along with the presence of putative GAGA binding sites within the slbo promoter and enhancer, suggests the direct regulation of this gene by GAGA. This idea is supported by the reduction in the slbo-Gal4-driven GFP expression within BC clusters in Trl mutant background. However, the inability of slbo overexpression to compensate defects in BC migration caused by Trl mutations suggests that there are other GAGA target genes contributing to this process. Taken together, the results define GAGA as another important regulator of BC migration in Drosophila oogenesis.

scholarly journals Analysis and Functional Verification of PoWRI1 Gene Associated with Oil Accumulation Process in Paeonia ostii

2021 ◽  
Vol 22 (13) ◽  
pp. 6996
Author(s):  
Jing Sun ◽  
Tian Chen ◽  
Mi Liu ◽  
Daqiu Zhao ◽  
Jun Tao
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Target Genes ◽  
De Novo ◽  
Fatty Acid Content ◽  
Functional Verification ◽  
Oil Accumulation ◽  
Reading Frame ◽  
Downstream Target ◽  
Expression Of Genes

The plant transcription factor WRINKLED1 (WRI1), a member of AP2/EREBP, is involved in the regulation of glycolysis and the expression of genes related to the de novo synthesis of fatty acids in plastids. In this study, the key regulator of seed oil synthesis and accumulation transcription factor gene PoWRI1 was identified and cloned, having a complete open reading frame of 1269 bp and encoding 422 amino acids. Subcellular localization analysis showed that PoWRI1 is located at the nucleus. After the expression vector of PoWRI1 was constructed and transformed into wild-type Arabidopsis thaliana, it was found that the overexpression of PoWRI1 increased the expression level of downstream target genes such as BCCP2, KAS1, and PKP-β1. As a result, the seeds of transgenic plants became larger, the oil content increased significantly, and the unsaturated fatty acid content increased, which provide a scientific theoretical basis for the subsequent use of genetic engineering methods to improve the fatty acid composition and content of plant seeds.

A novel fibroblast growth factor gene expressed in the developing nervous system is a downstream target of the chimeric homeodomain oncoprotein E2A-Pbx1

Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3221-3232 ◽  
Author(s):  
J.R. McWhirter ◽  
M. Goulding ◽  
J.A. Weiner ◽  
J. Chun ◽  
C. Murre
Keyword(s):  
Nervous System ◽  
Transcription Factor ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Target Genes ◽  
Representational Difference Analysis ◽  
Bhlh Transcription Factor ◽  
Fibroblast Growth ◽  
Downstream Target ◽  
Developing Nervous System

Pbx1 is a homeodomain transcription factor that has the ability to form heterodimers with homeodomain proteins encoded by the homeotic selector (Hox) gene complexes and increase their DNA-binding affinity and specificity. A current hypothesis proposes that interactions with Pbx1 are necessary for Hox proteins to regulate downstream target genes that in turn control growth, differentiation and morphogenesis during development. In pre B cell leukemias containing the t(1;19) chromosome translocation, Pbx1 is converted into a strong transactivator by fusion to the activation domain of the bHLH transcription factor E2A. The E2A-Pbx1 fusion protein should therefore activate transcription of genes normally regulated by Pbx1. We have used the subtractive process of representational difference analysis to identify targets of E2A-Pbx1. We show that E2A-Pbx1 can directly activate transcription of a novel member of the fibroblast growth factor family of intercellular signalling molecules, FGF-15. The FGF-15 gene is expressed in a regionally restricted pattern in the developing nervous system, suggesting that FGF-15 may play an important role in regulating cell division and patterning within specific regions of the embryonic brain, spinal cord and sensory organs.

ThejingZn-finger transcription factor is a mediator of cellular differentiation in theDrosophilaCNS midline and trachea

Development ◽  
2002 ◽  
Vol 129 (11) ◽  
pp. 2591-2606 ◽  
Author(s):  
Yalda Sedaghat ◽  
Wilson F. Miranda ◽  
Margaret J. Sonnenfeld
Keyword(s):  
Transcription Factor ◽  
Cellular Differentiation ◽  
Target Genes ◽  
Marker Gene ◽  
Downstream Target ◽  
Tracheal Cell ◽  
Marker Gene Expression ◽  
Embryonic Cns ◽  
Cns Midline ◽  
Drosophila Embryos

We establish that the jing zinc-finger transcription factor plays an essential role in controlling CNS midline and tracheal cell differentiation. jing transcripts and protein accumulate from stage 9 in the CNS midline, trachea and in segmental ectodermal stripes. JING protein localizes to the nuclei of CNS midline and tracheal cells implying a regulatory role during their development. Loss of jing-lacZ expression in homozygous sim mutants and induction of jing-lacZ by ectopic sim expression establish that jing is part of the CNS midline lineage. We have isolated embryonic recessive lethal jing mutations that display genetic interactions in the embryonic CNS midline and trachea, with mutations in the bHLH-PAS genes single-minded and trachealess, and their downstream target genes (slit and breathless). Loss- and gain-of-function jing is associated with defects in CNS axon and tracheal tubule patterning. In jing homozygous mutant embryos, reductions in marker gene expression and inappropriate apoptosis in the CNS midline and trachea establish that jing is essential for the proper differentiation and survival of these lineages. These results establish that jing is a key component of CNS midline and tracheal cell development. Given the similarities between JING and the vertebrate CCAAT-binding protein AEBP2, we propose that jing regulates transcriptional mechanisms in Drosophila embryos and promotes cellular differentiation in ectodermal derivatives.

scholarly journals Identification and analysis of KLF13 variants in patients with congenital heart disease

2019 ◽  
Author(s):  
Wenjuan Li ◽  
Baolei Li ◽  
Tingting Li ◽  
Ergeng Zhang ◽  
Qingjie Wang ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Transcription Factor ◽  
Heart Disease ◽  
Subcellular Localization ◽  
Protein Expression ◽  
Heart Development ◽  
Congenital Heart ◽  
Target Genes ◽  
Healthy Controls ◽  
Downstream Target

Abstract Background: The protein Kruppel-like factor 13 (KLF13) is a member of the KLF family that has been identified as a novel cardiac transcription factor which is involved in heart development. However, the relationship between KLF13 variants and CHDs in humans remains largely unknown. The present study aimed to screen the KLF13 variants in CHDs patients and genetically analyze the function of these variants. Methods: KLF13 variants were sequenced in a cohort of 309 CHD patients and population-matched healthy controls (n = 200) using targeted sequencing. To investigate the effect of variants on the functional ability of the KLF13 protein, the expressions and subcellular localization of protein, as well as the transcriptional activities of downstream genes and physically interacted with other transcription factor were assessed. Results: Two novel heterozygous variants, c.487C>T (P163S) and c.467G>A (S156N), were identified in two out of 309 CHDs patients with Tricuspid-valve atresia and transposition of the great arteries, respectively. No variants were found among healthy controls. The variant c.467G>A (S156N) increased protein expression and enhanced functionality compared with that of wild-type, without affecting the subcellular localization. The other variant, c.487C>T (P163S), did not show any abnormalities in protein expression and subcellular localization, however it eliminated the transcriptional activities of downstream target genes and physically interacted with TBX5, another cardiac transcription factor. Conclusion: Our results show that the S156N and P163S variants contributed to CHD etiology. Additionally, our findings suggest that KLF13 may be a potential gene contributing to congenital heart disease.

Abstract 066: MEF2-induced Loss of Sarcomeres is Mediated by an Alternative Splice Variant of DMPK

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Ies Elzenaar ◽  
Inge van der Made ◽  
Wino J Wijnen ◽  
Elisabeth Ehler ◽  
Leon J De Windt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Transcription Factor ◽  
Microarray Analysis ◽  
Splice Variant ◽  
Transcriptional Activity ◽  
Target Genes ◽  
Neonatal Rat ◽  
Pcr Analysis ◽  
Mrna Levels ◽  
Rat Cardiomyocytes

The pathology of heart failure is characterized by poorly contracting and dilated ventricles. Although this is associated with lengthening of individual cardiomyocytes and loss of sarcomeres, the mechanism underlying these changes in cardiomyocyte structure remains to be elucidated. We have previously identified the transcription factor myocyte enhancer factor-2 (MEF2) as important trigger for adverse cardiomyocyte remodeling. Here, we use microarray analysis and gain- and loss- of function approaches to identify MEF2 target genes involved in structural remodeling of the cardiomyocyte. Isolated neonatal rat cardiomyocytes infected with adenoviruses expressing MEF2 underwent cellular elongation associated with loss of sarcomeric structure. Microarray analysis revealed myotonic dystrophy protein kinase (DMPK) as MEF2 target gene, which we verified by chromatin immunoprecipitation experiments. siRNA mediated knockdown of DMPK prevented MEF2-induced cardiomyocyte elongation and loss of sarcomeres. Interestingly, RT-PCR analysis of known DMPK splice variants demonstrated a relative increase of the DMPK E isoform in failing mouse hearts. To test the role of this specific splice isoform, we generated adenoviruses expressing DMPK E or a kinase dead mutant DMPK E. Overexpression of wildtype DMPK E, but not of the kinase dead mutant, in cardiomyocytes resulted in severe loss of sarcomeric structure. Moreover, quantitative PCR analysis showed a decrease in mRNA levels for several sarcomeric genes after overexpression of DMPK E. These genes are known targets of the transcription factor serum response factor (SRF) and DMPK is known to phosphorylate SRF. Therefore, we tested the effect of DMPK on SRF activity in luciferase experiments, which demonstrated that DMPK E is an inhibitor of SRF transcriptional activity. Our data indicate that MEF2 induces loss of sarcomeres, which is mediated by at least one specific splice variant of DMPK. Moreover, increased expression of this DMPK splice variant results in a decrease in sarcomeric gene expression, which possibly involves inhibition of SRF transcriptional activity. Together, these results assign a novel function to MEF2 and DMPK in adverse cardiomyocyte remodeling during heart failure development.

Expression of AP-2 transcription factor and of its downstream target genes c-kit, E-cadherin and p21 in human cutaneous melanoma

2001 ◽  
Vol 83 (3) ◽  
pp. 364-372 ◽  
Author(s):  
Alfonso Baldi ◽  
Daniele Santini ◽  
Tullio Battista ◽  
Emanuele Dragonetti ◽  
Giulio Ferranti ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cutaneous Melanoma ◽  
Target Genes ◽  
Downstream Target ◽  
E Cadherin

Treatment with bevacizumab (BEV) upregulates expression of the transcription factor Sp1 and its downstream target genes in human carcinoid cells: Molecular basis of the synergistic antiangiogenic activity of bevacizumab and mithramycin A (MIT)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 15031-15031 ◽  
Author(s):  
J. Zhang ◽  
Z. Jia ◽  
L. Wang ◽  
Q. Li ◽  
L. Xiangdong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Growth Factor ◽  
Nude Mice ◽  
Target Genes ◽  
Critical Role ◽  
Angiogenic Factors ◽  
Downstream Target ◽  
Transcription Factor Sp1 ◽  
Mithramycin A ◽  
The Impact

15031 Background: Our previous studies show that human carcinoid cells overexpress pro-angiogenic factors, vascular endothelial growth factor A (VEGF), and transcription factor Sp1 plays a critical role in VEGF inducible and constitutive expression. However, the impact of antiangiogenic therapy on the Sp1/VEGF pathway remains unclear. Method: Groups of 10 athymic BALB/c nude mice were implanted with 1.5 million human H727 carcinoid cells. Treatment with VEGF neutralizing monoclonal antibody, BEV, MIT, or BEV + MIT was initiated once implanted tumor reached 4 mm in size. Result: Treatment with BEV, suppressed human carcinoid growth in nude mice (tumor size at week 5 1280 mm3 vs 480 mm3; p < 0.001). Gene expression analyses revealed that this treatment substantially upregulated the expression of Sp1 (7 folds) and its downstream target genes, including VEGF (5 folds) and epidermal growth factor receptor (4 folds), in tumor tissues, whereas it did not have this effect on carcinoid cells in culture. Treatment with mithramycin A, an Sp1 inhibitor, suppressed the expression of Sp1 and its downstream target genes in both cell culture and tumors growing in nude mice. Median survival of mice treated with PBS, BEV, MIT, and BEV + MIT groups were 88, 112, 121, and >160 days respectively (p < 0.001). Combined treatment with bevacizumab and mithramycin A produced synergistic tumor suppression, which was consistent with suppression of the expression of Sp1 and its downstream target genes. Conclusion: Treatment with bevacizumab may block VEGF function but activate the pathway of its expression via positive feedback. Given the fact that Sp1 is an important regulator of the expression of multiple angiogenic factors, bevacizumab-initiated upregulation of Sp1 and subsequent overexpression of its downstream target genes may affect the potential angiogenic phenotype and effectiveness of antiangiogenic strategies for human carcinoid. No significant financial relationships to disclose.

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