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Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis

Kruppel-like factor 4 (Klf4) is a zinc finger transcription factor and plays crucial roles in Xenopus embryogenesis. However, its regulation during embryogenesis is still unclear. Here, we report that Tcf7l1, a key downstream transducer of the Wnt signaling pathway, could promote Klf4 transcription...

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Detalles Bibliográficos
Autores principales: Cao, Qing, Shen, Yan, Zheng, Wei, Liu, Hao, Liu, Chen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Editorial Department of Journal of Biomedical Research 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6265397/
https://www.ncbi.nlm.nih.gov/pubmed/29336356
http://dx.doi.org/10.7555/JBR.32.20170056
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author Cao, Qing
Shen, Yan
Zheng, Wei
Liu, Hao
Liu, Chen
author_facet Cao, Qing
Shen, Yan
Zheng, Wei
Liu, Hao
Liu, Chen
author_sort Cao, Qing
collection PubMed
description Kruppel-like factor 4 (Klf4) is a zinc finger transcription factor and plays crucial roles in Xenopus embryogenesis. However, its regulation during embryogenesis is still unclear. Here, we report that Tcf7l1, a key downstream transducer of the Wnt signaling pathway, could promote Klf4 transcription and stimulate Klf4 promoter activity in early Xenopus embryos. Furthermore, cycloheximide treatment showed a direct effect on Klf4 transcription facilitated by Tcf7l1. Moreover, the dominant negative form of Tcf7l1 (dnTcf7l1), which lacks N-terminus of the β-catenin binding motif, could still activate Klf4 transcription, suggesting that this regulation is Wnt/β-catenin independent. Taken together, our results demonstrate that Tcf7l1 lies upstream of Klf4 to maintain its expression level during Xenopus embryogenesis.
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spelling pubmed-62653972018-12-11 Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis Cao, Qing Shen, Yan Zheng, Wei Liu, Hao Liu, Chen J Biomed Res Original Article Kruppel-like factor 4 (Klf4) is a zinc finger transcription factor and plays crucial roles in Xenopus embryogenesis. However, its regulation during embryogenesis is still unclear. Here, we report that Tcf7l1, a key downstream transducer of the Wnt signaling pathway, could promote Klf4 transcription and stimulate Klf4 promoter activity in early Xenopus embryos. Furthermore, cycloheximide treatment showed a direct effect on Klf4 transcription facilitated by Tcf7l1. Moreover, the dominant negative form of Tcf7l1 (dnTcf7l1), which lacks N-terminus of the β-catenin binding motif, could still activate Klf4 transcription, suggesting that this regulation is Wnt/β-catenin independent. Taken together, our results demonstrate that Tcf7l1 lies upstream of Klf4 to maintain its expression level during Xenopus embryogenesis. Editorial Department of Journal of Biomedical Research 2018-06-26 2017-11-30 /pmc/articles/PMC6265397/ /pubmed/29336356 http://dx.doi.org/10.7555/JBR.32.20170056 Text en © 2018 by the Journal of Biomedical Research. All rights reserved /creativecommons.org/licenses/by/4.0/ This is an open access article under the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited.
spellingShingle Original Article
Cao, Qing
Shen, Yan
Zheng, Wei
Liu, Hao
Liu, Chen
Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title_full Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title_fullStr Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title_full_unstemmed Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title_short Tcf7l1 promotes transcription of Kruppel-like factor 4 during Xenopus embryogenesis
title_sort tcf7l1 promotes transcription of kruppel-like factor 4 during xenopus embryogenesis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6265397/
https://www.ncbi.nlm.nih.gov/pubmed/29336356
http://dx.doi.org/10.7555/JBR.32.20170056
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