An extended transcription factor regulatory network controls hepatocyte identity

Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network contro...

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Published inEMBO reports Vol. 24; no. 9; p. e57020
Main Authors Dubois‐Chevalier, Julie, Gheeraert, Céline, Berthier, Alexandre, Boulet, Clémence, Dubois, Vanessa, Guille, Loïc, Fourcot, Marie, Marot, Guillemette, Gauthier, Karine, Dubuquoy, Laurent, Staels, Bart, Lefebvre, Philippe, Eeckhoute, Jérôme
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 06.09.2023
Springer Nature B.V
EMBO Press
John Wiley and Sons Inc
Subjects
Circuits
EMBO09
EMBO24
Gene expression
Gene regulation
Hepatocellular carcinoma
Hepatocytes
Inflammation
Life Sciences
Liver
Receptors
Thyroid
Thyroid gland
Transcription factors
cell identity
core regulatory network
liver disease
transcription factors
hepatocyte dedifferentiation
transcription factors Subject Categories Transcription & Genomics
cell identity core regulatory network hepatocyte dedifferentiation liver disease transcription factors Subject Categories Transcription & Genomics Molecular Biology of Disease
Molecular Biology of Disease
Online AccessGet full text
ISSN1469-221X
1469-3178
1469-3178
DOI10.15252/embr.202357020

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Abstract Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non‐cell‐specific TFs beyond the CoRC, which we call hepatocyte identity (Hep‐ID) CONNECT TFs. Besides controlling identity effector genes, Hep‐ID CONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep‐ID CONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep‐ID CONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep‐ID CONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation‐induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC. Synopsis Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes. Hepatocyte identity TFs of the CoRC are tightly connected to a large set of non‐hepatocyte‐specific TFs that we call Hep‐IDCONNECT TFs Hep‐IDCONNECT TFs fine tune hepatocyte identity TF expression in homeostatic basal conditions In dedifferentiated hepatocytes, Hep‐IDCONNECT TFs can reset hepatocyte identity as shown for the thyroid hormone receptor beta whose activation induces expression of the CoRC TFs in hepatocarcinoma and in hepatocytes subjected to inflammation‐induced loss of identity. Graphical Abstract Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes.
AbstractList Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non‐cell‐specific TFs beyond the CoRC, which we call hepatocyte identity (Hep‐ID)CONNECT TFs. Besides controlling identity effector genes, Hep‐IDCONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep‐IDCONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep‐IDCONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep‐IDCONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation‐induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell-specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non-cell-specific TFs beyond the CoRC, which we call hepatocyte identity (Hep-ID) CONNECT TFs. Besides controlling identity effector genes, Hep-ID CONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep-ID CONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep-ID CONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep-ID CONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammationinduced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non‐cell‐specific TFs beyond the CoRC, which we call hepatocyte identity (Hep‐ID)CONNECT TFs. Besides controlling identity effector genes, Hep‐IDCONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep‐IDCONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep‐IDCONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep‐IDCONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation‐induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC. Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non‐cell‐specific TFs beyond the CoRC, which we call hepatocyte identity (Hep‐ID) CONNECT TFs. Besides controlling identity effector genes, Hep‐ID CONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep‐ID CONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep‐ID CONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep‐ID CONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation‐induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC. Synopsis Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes. Hepatocyte identity TFs of the CoRC are tightly connected to a large set of non‐hepatocyte‐specific TFs that we call Hep‐IDCONNECT TFs Hep‐IDCONNECT TFs fine tune hepatocyte identity TF expression in homeostatic basal conditions In dedifferentiated hepatocytes, Hep‐IDCONNECT TFs can reset hepatocyte identity as shown for the thyroid hormone receptor beta whose activation induces expression of the CoRC TFs in hepatocarcinoma and in hepatocytes subjected to inflammation‐induced loss of identity. Graphical Abstract Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell-specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non-cell-specific TFs beyond the CoRC, which we call hepatocyte identity (Hep-ID) TFs. Besides controlling identity effector genes, Hep-ID TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep-ID TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep-ID TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep-ID TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation-induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell-specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non-cell-specific TFs beyond the CoRC, which we call hepatocyte identity (Hep-ID)CONNECT TFs. Besides controlling identity effector genes, Hep-IDCONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep-IDCONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep-IDCONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep-IDCONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation-induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC.Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell-specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non-cell-specific TFs beyond the CoRC, which we call hepatocyte identity (Hep-ID)CONNECT TFs. Besides controlling identity effector genes, Hep-IDCONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep-IDCONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep-IDCONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep-IDCONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation-induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC.
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific transcription factors (TFs). By mining global hepatic TF regulons, we reveal a more complex organization of the transcriptional regulatory network controlling hepatocyte identity. We show that tight functional interconnections controlling hepatocyte identity extend to non‐cell‐specific TFs beyond the CoRC, which we call hepatocyte identity (Hep‐ID) CONNECT TFs. Besides controlling identity effector genes, Hep‐ID CONNECT TFs also engage in reciprocal transcriptional regulation with TFs of the CoRC. In homeostatic basal conditions, this translates into Hep‐ID CONNECT TFs being involved in fine tuning CoRC TF expression including their rhythmic expression patterns. Moreover, a role for Hep‐ID CONNECT TFs in the control of hepatocyte identity is revealed in dedifferentiated hepatocytes where Hep‐ID CONNECT TFs are able to reset CoRC TF expression. This is observed upon activation of NR1H3 or THRB in hepatocarcinoma or in hepatocytes subjected to inflammation‐induced loss of identity. Our study establishes that hepatocyte identity is controlled by an extended array of TFs beyond the CoRC. image Hepatocyte identity is controlled by interconnected transcription factors (TFs) extending beyond the core regulatory TF network (CoRC). The extended network comprises thyroid hormone receptor beta whose activation resets CoRC TFs expression and hepatocyte identity in dedifferentiated hepatocytes. Hepatocyte identity TFs of the CoRC are tightly connected to a large set of non‐hepatocyte‐specific TFs that we call Hep‐IDCONNECT TFs Hep‐IDCONNECT TFs fine tune hepatocyte identity TF expression in homeostatic basal conditions In dedifferentiated hepatocytes, Hep‐IDCONNECT TFs can reset hepatocyte identity as shown for the thyroid hormone receptor beta whose activation induces expression of the CoRC TFs in hepatocarcinoma and in hepatocytes subjected to inflammation‐induced loss of identity.
Author Boulet, Clémence
Lefebvre, Philippe
Marot, Guillemette
Berthier, Alexandre
Dubois, Vanessa
Dubuquoy, Laurent
Guille, Loïc
Staels, Bart
Fourcot, Marie
Dubois‐Chevalier, Julie
Eeckhoute, Jérôme
Gheeraert, Céline
Gauthier, Karine
AuthorAffiliation 3 Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, US 41 – UAR 2014 – PLBS Lille France
1 Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011‐EGID Lille France
2 Basic and Translational Endocrinology (BaTE), Department of Basic and Applied Medical Sciences Ghent University Ghent Belgium
4 Univ. Lille, Inria, CHU Lille, ULR 2694 – METRICS: Évaluation des technologies de santé et des pratiques médicales Lille France
5 Institut de Génomique Fonctionnelle de Lyon (IGFL), CNRS UMR 5242, INRAE USC 1370, École Normale Supérieure de Lyon Lyon France
6 Univ. Lille, Inserm, CHU Lille, U1286 – INFINITE – Institute for Translational Research in Inflammation Lille France
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CitedBy_id crossref_primary_10_1136_gutjnl_2023_331741
crossref_primary_10_1111_cpr_13772
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– fundername: Agence Nationale de la Recherche (ANR)
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Issue 9
Keywords cell identity
core regulatory network
liver disease
transcription factors
hepatocyte dedifferentiation
transcription factors Subject Categories Transcription & Genomics
cell identity core regulatory network hepatocyte dedifferentiation liver disease transcription factors Subject Categories Transcription & Genomics Molecular Biology of Disease
Molecular Biology of Disease
Language English
License 2023 The Authors. Published under the terms of the CC BY 4.0 license.
Attribution: http://creativecommons.org/licenses/by
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
cc-by
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Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
These authors contributed equally to this work
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Snippet Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell‐specific...
Cell identity is specified by a core transcriptional regulatory circuitry (CoRC), typically limited to a small set of interconnected cell-specific...
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SubjectTerms Circuits
EMBO09
EMBO24
Gene expression
Gene regulation
Hepatocellular carcinoma
Hepatocytes
Inflammation
Life Sciences
Liver
Receptors
Thyroid
Thyroid gland
Transcription factors
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Title An extended transcription factor regulatory network controls hepatocyte identity
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