scholarly journals The Cdx transcription factors and retinoic acid play parallel roles in antero-posterior position of the pectoral fin field during gastrulation

2020 ◽  
Vol 164 ◽  
pp. 103644
Author(s):  
Christopher A. Quintanilla ◽  
Robert K. Ho
Keyword(s):  
Transcription Factors ◽  
Retinoic Acid ◽  
Pectoral Fin ◽  
Posterior Position

scholarly journals Nicotine, IFN-γ and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades

2012 ◽  
Vol 11 (1) ◽  
pp. 24 ◽  
Author(s):  
Sateesh Kunigal ◽  
Moorthy P Ponnusamy ◽  
Navneet Momi ◽  
Surinder K Batra ◽  
Srikumar P Chellappan
Keyword(s):  
Pancreatic Cancer ◽  
Transcription Factors ◽  
Retinoic Acid ◽  
Signaling Cascades ◽  
Ifn Γ

scholarly journals Mechanisms of Hox gene colinearity: transposition of the anterior Hoxb1 gene into the posterior HoxD complex

2000 ◽  
Vol 14 (2) ◽  
pp. 198-211 ◽  
Author(s):  
Marie Kmita ◽  
Frank van der Hoeven ◽  
József Zákány ◽  
Robb Krumlauf ◽  
Denis Duboule
Keyword(s):  
Retinoic Acid ◽  
Reporter Gene ◽  
General Property ◽  
Transgene Expression ◽  
Specific Activity ◽  
Hox Gene ◽  
Position Analysis ◽  
Ectopic Activation ◽  
Posterior Position ◽  
Gene Colinearity

Transposition of Hoxd genes to a more posterior (5′) location within the HoxD complex suggested that colinearity in the expression of these genes was due, in part, to the existence of a silencing mechanism originating at the 5′ end of the cluster and extending towards the 3′ direction. To assess the strength and specificity of this repression, as well as to challenge available models on colinearity, we inserted a Hoxb1/lacZtransgene within the posterior HoxD complex, thereby reconstructing a cluster with a copy of the most anterior gene inserted at the most posterior position. Analysis of Hoxb1 expression after ectopic relocation revealed that Hoxb1-specific activity in the fourth rhombomere was totally abolished. Treatment with retinoic acid, or subsequent relocations toward more 3′ positions in theHoxD complex, did not release this silencing in hindbrain cells. In contrast, however, early and anterior transgene expression in the mesoderm was unexpectedly not suppressed. Furthermore, the transgene induced a transient ectopic activation of the neighboringHoxd13 gene, without affecting other genes of the complex. Such a local and transient break in colinearity was also observed after transposition of the Hoxd9/lacZ reporter gene, indicating that it may be a general property of these transgenes when transposed at an ectopic location. These results are discussed in the context of existing models, which account for colinear activation of vertebrate Hox genes.

scholarly journals Cooperation of Cytokine Signaling with Chimeric Transcription Factors in Leukemogenesis: PML-Retinoic Acid Receptor Alpha Blocks Growth Factor-Mediated Differentiation

2003 ◽  
Vol 23 (13) ◽  
pp. 4573-4585 ◽  
Author(s):  
Vernon T. Phan ◽  
David B. Shultz ◽  
Bao-Tran H. Truong ◽  
Timothy J. Blake ◽  
Anna L. Brown ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Transcription Factors ◽  
Retinoic Acid ◽  
Myeloid Leukemia ◽  
Retinoic Acid Receptor ◽  
Promyelocytic Leukemia ◽  
Cytokine Signaling ◽  
Retinoic Acid Receptor Alpha ◽  
Acid Receptor ◽  
Acute Myeloid

ABSTRACT We utilized a mouse model of acute promyelocytic leukemia (APL) to investigate how aberrant activation of cytokine signaling pathways interacts with chimeric transcription factors to generate acute myeloid leukemia. Expression in mice of the APL-associated fusion, PML-RARA, initially has only modest effects on myelopoiesis. Whereas treatment of control animals with interleukin-3 (IL-3) resulted in expanded myelopoiesis without a block in differentiation, PML-RARA abrogated differentiation that normally characterizes the response to IL-3. Retroviral transduction of bone marrow with an IL-3-expressing retrovirus revealed that IL-3 and promyelocytic leukemia-retinoic acid receptor alpha (PML-RARα) combined to generate a lethal leukemia-like syndrome in <21 days. We also observed that a constitutively activated mutant IL-3 receptor, βcV449E, cooperated with PML-RARα in leukemogenesis, whereas a different activated mutant, βcI374N, did not. Analysis of additional mutations introduced into βcV449E showed that, although tyrosine phosphorylation of βc is necessary for cooperation, the Src homology 2 domain-containing transforming protein binding site is dispensable. Our results indicate that chimeric transcription factors can block the differentiative effects of growth factors. This combination can be potently leukemogenic, but the particular manner in which these types of mutations interact determines the ability of such combinations to generate acute myeloid leukemia.

scholarly journals A dynamic balance between ARP-1/COUP-TFII, EAR-3/COUP-TFI, and retinoic acid receptor:retinoid X receptor heterodimers regulates Oct-3/4 expression in embryonal carcinoma cells.

1995 ◽  
Vol 15 (2) ◽  
pp. 1034-1048 ◽  
Author(s):  
E Ben-Shushan ◽  
H Sharir ◽  
E Pikarsky ◽  
Y Bergman
Keyword(s):  
Transcription Factors ◽  
Retinoic Acid ◽  
Binding Site ◽  
Transcriptional Repression ◽  
Embryonal Carcinoma ◽  
Dependent Manner ◽  
Orphan Receptors ◽  
Positive Regulators ◽  
Ec Cells ◽  
Kinetics Of

The Oct-3/4 transcription factor is a member of the POU family of transcription factors and, as such, probably plays a crucial role in mammalian embryogenesis and differentiation. It is expressed in the earliest stages of embryogenesis and repressed in subsequent stages. Similarly, Oct-3/4 is expressed in embryonal carcinoma (EC) cells and is repressed in retinoic acid (RA)-differentiated EC cells. Previously we have shown that the Oct-3/4 promoter harbors an RA-responsive element, RAREoct, which functions in EC cells as a binding site for positive regulators of transcription and in RA-differentiated EC cells as a binding site for positive regulators of transcription and in RA-differentiated EC cells as a binding site for negative regulators. Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. While the N-terminal region of the ARP-1/COUP-TFII receptor is dispensable for this repression, the C-terminal domain harbors the silencing region. Interestingly, three different RA receptor:retinoid X receptor (RAR:RXR) heterodimers, RAR alpha:RXR alpha, RAR beta:RXR alpha, and RAR beta:RXR beta, specifically bind and activate Oct-3/4 promoter through the RAREoct site in a ligand-dependent manner. We have shown that antagonism between ARP-1/COUP-TFII or EAR-3/COUP-TFI and the RAR:RXR heterodimers and their intracellular balance modulate Oct-3/4 expression. Oct-3/4 transcriptional repression by the orphan receptors can be overcome by increasing amounts of RAR:RXR heterodimers. Conversely, activation of Oct-3/4 promoter by RAR:RXR heterodimers was completely abolished by EAR-3/COUP-TFI and by ARP-1/COUP-TFII. The orphan receptors bind the RAREoct site with a much higher affinity than the RAR:RXR heterodimers. This high binding affinity provides ARP-1/COUP-TFII and EAR-3/COUP-TFI with the ability to compete with and even displace RAR:RXR from the RAREoct site and subsequently to actively silence the Oct-3/4 promoter. We have shown that RA treatment of EC cells results in up-regulation of ARP-1/COUP-TFII and EAR-3/COUP-TFI expression. Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. These findings are in accordance with the suggestion that these orphan receptors participate in controlling a network of transcription factors, among which Oct-3/4 is included, which may establish the pattern of normal gene expression during development.

scholarly journals Establishing sharp and homogeneous segments in the hindbrain

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1268 ◽  
Author(s):  
David G. Wilkinson
Keyword(s):  
Transcription Factors ◽  
Retinoic Acid ◽  
Regional Identity ◽  
Parallel Mechanisms ◽  
Cell Identity ◽  
Dynamic Regulation ◽  
Retinoic Acid Signalling ◽  
Early Stages ◽  
Cell Segregation ◽  
Segmental Identity

Studies of the vertebrate hindbrain have revealed parallel mechanisms that establish sharp segments with a distinct and homogeneous regional identity. Recent work has revealed roles of cell identity regulation and its relationships with cell segregation. At early stages, there is overlapping expression at segment borders of the Egr2 and Hoxb1 transcription factors that specify distinct identities, which is resolved by reciprocal repression. Computer simulations show that this dynamic regulation of cell identity synergises with cell segregation to generate sharp borders. Some intermingling between segments occurs at early stages, and ectopic egr2-expressing cells switch identity to match their new neighbours. This switching is mediated by coupling between egr2 expression and the level of retinoic acid signalling, which acts in a community effect to maintain homogeneous segmental identity. These findings reveal an interplay between cell segregation and the dynamic regulation of cell identity in the formation of sharp patterns in the hindbrain and raise the question of whether similar mechanisms occur in other tissues.

scholarly journals Axial skeleton anterior-posterior patterning is regulated through feedback regulation between Meis transcription factors and retinoic acid

Development ◽  
2020 ◽  
Vol 148 (1) ◽  
pp. dev193813
Author(s):  
Alejandra C. López-Delgado ◽  
Irene Delgado ◽  
Vanessa Cadenas ◽  
Fátima Sánchez-Cabo ◽  
Miguel Torres
Keyword(s):  
Transcription Factors ◽  
Retinoic Acid ◽  
Hox Genes ◽  
Feedback Regulation ◽  
Axial Skeleton ◽  
Paraxial Mesoderm ◽  
Hox Proteins ◽  
Skeletal Defects ◽  
Hox Protein ◽  
Anterior Posterior

ABSTRACTVertebrate axial skeletal patterning is controlled by co-linear expression of Hox genes and axial level-dependent activity of HOX protein combinations. MEIS transcription factors act as co-factors of HOX proteins and profusely bind to Hox complex DNA; however, their roles in mammalian axial patterning remain unknown. Retinoic acid (RA) is known to regulate axial skeletal element identity through the transcriptional activity of its receptors; however, whether this role is related to MEIS/HOX activity remains unknown. Here, we study the role of Meis in axial skeleton formation and its relationship to the RA pathway in mice. Meis elimination in the paraxial mesoderm produces anterior homeotic transformations and rib mis-patterning associated to alterations of the hypaxial myotome. Although Raldh2 and Meis positively regulate each other, Raldh2 elimination largely recapitulates the defects associated with Meis deficiency, and Meis overexpression rescues the axial skeletal defects in Raldh2 mutants. We propose a Meis-RA-positive feedback loop, the output of which is Meis levels, that is essential to establish anterior-posterior identities and patterning of the vertebrate axial skeleton.

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