scholarly journals Differential binding of the related transcription factors Pho4 and Cbf1 can tune the sensitivity of promoters to different levels of an induction signal

2013 ◽  
Vol 41 (9) ◽  
pp. 4877-4887 ◽  
Author(s):  
Jonathan S. Z. Aow ◽  
Xiaowei Xue ◽  
Jin-Quan Run ◽  
Geoffrey F. S. Lim ◽  
Wee Siong Goh ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Induction Signal ◽  
Differential Binding ◽  
Different Levels

scholarly journals Class I TCP transcription factors regulate trichome branching and cuticle development in Arabidopsis

2020 ◽  
Vol 71 (18) ◽  
pp. 5438-5453
Author(s):  
Alejandra Camoirano ◽  
Agustín L Arce ◽  
Federico D Ariel ◽  
Antonela L Alem ◽  
Daniel H Gonzalez ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Regulatory Network ◽  
Class I ◽  
Branch Number ◽  
Plant Organ ◽  
Cuticle Formation ◽  
Cuticle Development ◽  
Different Levels

Abstract Trichomes and the cuticle are two specialized structures of the aerial epidermis that are important for plant organ development and interaction with the environment. In this study, we report that Arabidopsis thaliana plants affected in the function of the class I TEOSINTE BRANCHED 1, CYCLOIDEA, PCF (TCP) transcription factors TCP14 and TCP15 show overbranched trichomes in leaves and stems and increased cuticle permeability. We found that TCP15 regulates the expression of MYB106, a MIXTA-like transcription factor involved in epidermal cell and cuticle development, and overexpression of MYB106 in a tcp14 tcp15 mutant reduces trichome branch number. TCP14 and TCP15 are also required for the expression of the cuticle biosynthesis genes CYP86A4, GPAT6, and CUS2, and of SHN1 and SHN2, two AP2/EREBP transcription factors required for cutin and wax biosynthesis. SHN1 and CUS2 are also targets of TCP15, indicating that class I TCPs influence cuticle formation acting at different levels, through the regulation of MIXTA-like and SHN transcription factors and of cuticle biosynthesis genes. Our study indicates that class I TCPs are coordinators of the regulatory network involved in trichome and cuticle development.

scholarly journals Differential Binding of the Transcription Factors Sp1, AP-1, and NFI to the Promoter of the Human α5 Integrin Gene Dictates Its Transcriptional Activity

2009 ◽  
Vol 50 (1) ◽  
pp. 57 ◽  
Author(s):  
Marie-E`ve Gingras ◽  
Be´ne´dicte Masson-Gadais ◽  
Karine Zaniolo ◽  
Steeve Leclerc ◽  
Re´gen Drouin ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activity ◽  
Integrin Gene ◽  
Differential Binding

scholarly journals AP1 Transcription Factors in Epidermal Differentiation and Skin Cancer

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Richard L. Eckert ◽  
Gautam Adhikary ◽  
Christina A. Young ◽  
Ralph Jans ◽  
James F. Crish ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Dominant Negative ◽  
Epidermal Differentiation ◽  
Cancer Development ◽  
Multiple Cells ◽  
Different Levels ◽  
Factor Function

AP1 (jun/fos) transcription factors (c-jun, junB, junD, c-fos, FosB, Fra-1, and Fra-2) are key regulators of epidermal keratinocyte survival and differentiation and important drivers of cancer development. Understanding the role of these factors in epidermis is complicated by the fact that each protein is expressed, at different levels, in multiple cells layers in differentiating epidermis, and because AP1 transcription factors regulate competing processes (i.e., proliferation, apoptosis, and differentiation). Variousin vivogenetic approaches have been used to study these proteins including targeted and conditional knockdown, overexpression, and expression of dominant-negative inactivating AP1 transcription factors in epidermis. Taken together, these studies suggest that individual AP1 transcription factors have different functions in the epidermis and in cancer development and that altering AP1 transcription factor function in the basal versus suprabasal layers differentially influences the epidermal differentiation response and disease and cancer development.

scholarly journals Activation of Haa1 and War1 transcription factors by differential binding of weak acid anions inSaccharomyces cerevisiae

2018 ◽  
Vol 47 (3) ◽  
pp. 1211-1224 ◽  
Author(s):  
Myung Sup Kim ◽  
Kyung Hee Cho ◽  
Kwang Hyun Park ◽  
Jyongsik Jang ◽  
Ji-Sook Hahn
Keyword(s):  
Transcription Factors ◽  
Weak Acid ◽  
Differential Binding

scholarly journals Mouse heat shock transcription factors 1 and 2 prefer a trimeric binding site but interact differently with the HSP70 heat shock element.

1993 ◽  
Vol 13 (6) ◽  
pp. 3370-3383 ◽  
Author(s):  
P E Kroeger ◽  
K D Sarge ◽  
R I Morimoto
Keyword(s):  
Transcription Factors ◽  
Heat Shock ◽  
Binding Site ◽  
Heat Shock Element ◽  
Heat Shock Transcription Factors ◽  
Adjacent Site ◽  
Differential Binding ◽  
Dyad Symmetry ◽  
Human Hsp70

To understand the function of multiple heat shock transcription factors in higher eukaryotes, we have characterized the interaction of recombinant mouse heat shock transcription factors 1 and 2 (mHSF1 and mHSF2) with their binding site, the heat shock element (HSE). For our analysis, we utilized the human HSP70 HSE, which consists of three perfect 5'-nGAAn-3' sites (1, 3, and 4) and two imperfect sites (2 and 5) arranged as tandem inverted repeats. Recombinant mHSF1 and mHSF2, which exist as trimers in solution, both bound specifically to this HSE and stimulated transcription of a human HSP70-CAT construct in vitro. Footprinting analyses revealed differential binding of mHSF1 and mHSF2 to the HSP70 HSE. Specifically, mHSF1 bound all five pentameric sites, whereas mHSF2 failed to interact with the first site of the HSE but bound to sites 2 to 5. Missing-nucleoside analysis demonstrated that the third and fourth nGAAn sites were essential for mHSF1 and mHSF2 binding. The binding of the initial mHSF1 trimer to the HSE exhibited preference for sites 3, 4, and 5, and then binding of a second trimer occurred at sites 1 and 2. These results suggest that HSF may recognize its binding site through the dyad symmetry of sites 3 and 4 but requires an adjacent site for stable interaction. Our data demonstrate that mHSF1 and mHSF2 bind specifically to the HSE through major groove interactions. Methidiumpropyl-EDTA footprinting revealed structural differences in the first and third repeats of the HSE, suggesting that the DNA is distorted in this region. The possibility that the HSE region is naturally distorted may assist in understanding how a trimer of HSF can bind to what is essentially an inverted repeat binding site.

scholarly journals Low Bone Turnover in Chronic Kidney Disease Is Associated with Decreased VEGF-A Expression and Osteoblast Differentiation

2015 ◽  
Vol 41 (6) ◽  
pp. 464-473 ◽  
Author(s):  
Neal X. Chen ◽  
Kalisha D. O''Neill ◽  
Matthew R. Allen ◽  
Christopher L. Newman ◽  
Sharon M. Moe
Keyword(s):  
Chronic Kidney Disease ◽  
Transcription Factors ◽  
Kidney Disease ◽  
Osteoblast Differentiation ◽  
Alternative Hypothesis ◽  
Hypoxia Inducible Factor ◽  
Low Bone Turnover ◽  
And Oxidative Stress ◽  
Different Levels ◽  
Pth Level

Background: Low turnover bone (low bone formation rates (BFRs)) with decreased osteoblast number is common in patients with chronic kidney disease (CKD) and attributed to ‘over-suppression' of the parathyroid hormone (PTH) despite supra-physiologic levels. An alternative hypothesis is abnormal osteoblast differentiation, resulting in low BFRs due to reduced VEGF-A. Methods: We analyzed the expression of VEGF-A and mesenchymal stem cell (MSC) differentiation factors in freshly isolated bone marrow (BM) cells, and in BM cell-derived MSC in rats with different levels of BFRs and PTH (modulated by calcium and zoledronic acid). The regulators of VEGF in MSC were also determined. Results: VEGF-A expression was reduced in the BM cells from CKD vs. normal animals (p < 0.02). In BM-derived MSC from CKD, there were decreased osteoblast transcription factors and mineralization. In CKD animals, the BM VEGF-A expression was positively correlated with BFR (r = 0.80, p < 0.001). Reducing BFRs in CKD animals led to reductions in VEGF-A expression and osteoblast transcription factors regardless of the PTH level. We therefore examined other regulators of VEGF-A and found decreased expression of hypoxia-inducible factor-1α and the master transcription factor of antioxidants nuclear factor (erythroid-derived 2)-like 2 in CKD animals with low PTH. Conclusion: Low BFRs in CKD are associated with a basal decrease in VEGF-A expression in BM that may be driven by altered hypoxia and oxidative stress.

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