Atypical Transcriptional Activation by TCF via a Zic Transcription Factor in C. elegans Neuronal Precursors

Autor: Pauline Mélénec, Magali Iché-Torres, Ute Rothbächer, Sabrina Murgan, Oliver Hobert, Willi Kari, Vincent Bertrand
Přispěvatelé: Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Transcriptional Activation
animal structures
Models
Neurological

[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Biology
TCF/LEF family
DNA-binding protein
Article
General Biochemistry
Genetics and Molecular Biology

Animals
Genetically Modified

03 medical and health sciences
0302 clinical medicine
Neural Stem Cells
Transcription (biology)
Basic Helix-Loop-Helix Transcription Factors
Animals
Binding site
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Mode of action
Wnt Signaling Pathway
Molecular Biology
Transcription factor
Body Patterning
030304 developmental biology
Homeodomain Proteins
0303 health sciences
Neuropeptides
High Mobility Group Proteins
Wnt signaling pathway
Cell Biology
biology.organism_classification
Molecular biology
DNA-Binding Proteins
TCF Transcription Factors
030217 neurology & neurosurgery
Transcription Factors
Developmental Biology
Zdroj: Developmental Cell
Developmental Cell, 2015, 33 (6), pp.737-45. ⟨10.1016/j.devcel.2015.04.018⟩
Developmental Cell, Elsevier, 2015, 33 (6), pp.737-45. ⟨10.1016/j.devcel.2015.04.018⟩
ISSN: 1534-5807
DOI: 10.1016/j.devcel.2015.04.018⟩
Popis: International audience; Transcription factors of the TCF family are key mediators of the Wnt/β-catenin pathway. TCF usually activates transcription on cis-regulatory elements containing TCF binding sites when the pathway is active and represses transcription when the pathway is inactive. However, some direct targets display an opposite regulation (activated by TCF in the absence of Wnt), but the mechanism behind this atypical regulation remains poorly characterized. Here, we use the cis-regulatory region of an opposite target gene, ttx-3, to dissect the mechanism of this atypical regulation. Using a combination of genetic, molecular, and biochemical experiments, we establish that, in the absence of Wnt pathway activation, TCF activates ttx-3 expression via a Zic binding site by forming a complex with a Zic transcription factor. This mechanism is later reinforced by specific bHLH factors. This study reveals an atypical mode of action for TCF that may apply to other binary decisions mediated by Wnt signaling.
Databáze: OpenAIRE