The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis

Abstract A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain gene expression patterns during hematopoiesis. In this network, transcription factors regulate each other and are involved in regulatory loops with microRNAs. The microRNA cluster miR-17-...

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Autores principales:	Annekarin Meyer, Stefanie Herkt, Heike Kunze-Schumacher, Nicole Kohrs, Julia Ringleb, Lucas Schneider, Olga N. Kuvardina, Thomas Oellerich, Björn Häupl, Andreas Krueger, Erhard Seifried, Halvard Bonig, Joern Lausen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/08a880929fb94f77a1ebe4c4ac5a8a3a
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spelling	oai:doaj.org-article:08a880929fb94f77a1ebe4c4ac5a8a3a2021-12-02T12:33:05ZThe transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis10.1038/s41598-020-78629-z2045-2322https://doaj.org/article/08a880929fb94f77a1ebe4c4ac5a8a3a2020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-78629-zhttps://doaj.org/toc/2045-2322Abstract A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain gene expression patterns during hematopoiesis. In this network, transcription factors regulate each other and are involved in regulatory loops with microRNAs. The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.Annekarin MeyerStefanie HerktHeike Kunze-SchumacherNicole KohrsJulia RinglebLucas SchneiderOlga N. KuvardinaThomas OellerichBjörn HäuplAndreas KruegerErhard SeifriedHalvard BonigJoern LausenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-17 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Annekarin Meyer Stefanie Herkt Heike Kunze-Schumacher Nicole Kohrs Julia Ringleb Lucas Schneider Olga N. Kuvardina Thomas Oellerich Björn Häupl Andreas Krueger Erhard Seifried Halvard Bonig Joern Lausen The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
description	Abstract A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain gene expression patterns during hematopoiesis. In this network, transcription factors regulate each other and are involved in regulatory loops with microRNAs. The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.
format	article
author	Annekarin Meyer Stefanie Herkt Heike Kunze-Schumacher Nicole Kohrs Julia Ringleb Lucas Schneider Olga N. Kuvardina Thomas Oellerich Björn Häupl Andreas Krueger Erhard Seifried Halvard Bonig Joern Lausen
author_facet	Annekarin Meyer Stefanie Herkt Heike Kunze-Schumacher Nicole Kohrs Julia Ringleb Lucas Schneider Olga N. Kuvardina Thomas Oellerich Björn Häupl Andreas Krueger Erhard Seifried Halvard Bonig Joern Lausen
author_sort	Annekarin Meyer
title	The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
title_short	The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
title_full	The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
title_fullStr	The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
title_full_unstemmed	The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis
title_sort	transcription factor tal1 and mir-17-92 create a regulatory loop in hematopoiesis
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/08a880929fb94f77a1ebe4c4ac5a8a3a
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The transcription factor TAL1 and miR-17-92 create a regulatory loop in hematopoiesis

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