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GATA3 induces human T-cell commitment by restraining Notch activity and repressing NK-cell fate

Inge Van de Walle, Anne-Catherine Dolens UGent, Kaat Durinck UGent, Katrien De Mulder, Wouter Van Loocke UGent, Sagar Damle, Els Waegemans, Jelle De Medts, Imke Velghe UGent, Magda De Smedt, et al. (2016) NATURE COMMUNICATIONS. 7.
abstract
The gradual reprogramming of haematopoietic precursors into the T-cell fate is characterized by at least two sequential developmental stages. Following Notch1-dependent T-cell lineage specification during which the first T-cell lineage genes are expressed and myeloid and dendritic cell potential is lost, T-cell specific transcription factors subsequently induce T-cell commitment by repressing residual natural killer (NK)-cell potential. How these processes are regulated in human is poorly understood, especially since efficient T-cell lineage commitment requires a reduction in Notch signalling activity following T-cell specification. Here, we show that GATA3, in contrast to TCF1, controls human T-cell lineage commitment through direct regulation of three distinct processes: repression of NK-cell fate, upregulation of T-cell lineage genes to promote further differentiation and restraint of Notch activity. Repression of the Notch1 target gene DTX1 hereby is essential to prevent NK-cell differentiation. Thus, GATA3-mediated positive and negative feedback mechanisms control human T-cell lineage commitment.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
MOUSE, ACUTE LYMPHOBLASTIC-LEUKEMIA, TARGET, CHECKPOINT, EXPRESSION, DIFFERENTIATION, ALPHA-BETA, TRANSCRIPTIONAL CONTROL, LINEAGE SPECIFICATION, RECEPTOR-LIGAND INTERACTIONS
journal title
NATURE COMMUNICATIONS
Nat. Commun.
volume
7
article number
11171
pages
14 pages
Web of Science type
Article
Web of Science id
000373822600001
JCR category
MULTIDISCIPLINARY SCIENCES
JCR impact factor
12.124 (2016)
JCR rank
3/64 (2016)
JCR quartile
1 (2016)
ISSN
2041-1723
DOI
10.1038/ncomms11171
language
English
UGent publication?
yes
classification
A1
copyright statement
Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
id
7249167
handle
http://hdl.handle.net/1854/LU-7249167
date created
2016-06-10 16:54:21
date last changed
2017-05-04 13:53:51
@article{7249167,
  abstract     = {The gradual reprogramming of haematopoietic precursors into the T-cell fate is characterized by at least two sequential developmental stages. Following Notch1-dependent T-cell lineage specification during which the first T-cell lineage genes are expressed and myeloid and dendritic cell potential is lost, T-cell specific transcription factors subsequently induce T-cell commitment by repressing residual natural killer (NK)-cell potential. How these processes are regulated in human is poorly understood, especially since efficient T-cell lineage commitment requires a reduction in Notch signalling activity following T-cell specification. Here, we show that GATA3, in contrast to TCF1, controls human T-cell lineage commitment through direct regulation of three distinct processes: repression of NK-cell fate, upregulation of T-cell lineage genes to promote further differentiation and restraint of Notch activity. Repression of the Notch1 target gene DTX1 hereby is essential to prevent NK-cell differentiation. Thus, GATA3-mediated positive and negative feedback mechanisms control human T-cell lineage commitment.},
  articleno    = {11171},
  author       = {Van de Walle, Inge and Dolens, Anne-Catherine and Durinck, Kaat and De Mulder, Katrien and Van Loocke, Wouter and Damle, Sagar and Waegemans, Els and De Medts, Jelle and Velghe, Imke and De Smedt, Magda and Vandekerckhove, Bart and Kerre, Tessa and Plum, Jean and Leclercq, Georges and Rothenberg, Ellen V and Van Vlierberghe, Pieter and Speleman, Franki and Taghon, Tom},
  issn         = {2041-1723},
  journal      = {NATURE COMMUNICATIONS},
  keyword      = {MOUSE,ACUTE LYMPHOBLASTIC-LEUKEMIA,TARGET,CHECKPOINT,EXPRESSION,DIFFERENTIATION,ALPHA-BETA,TRANSCRIPTIONAL CONTROL,LINEAGE SPECIFICATION,RECEPTOR-LIGAND INTERACTIONS},
  language     = {eng},
  pages        = {14},
  title        = {GATA3 induces human T-cell commitment by restraining Notch activity and repressing NK-cell fate},
  url          = {http://dx.doi.org/10.1038/ncomms11171},
  volume       = {7},
  year         = {2016},
}

Chicago
Van de Walle, Inge, Anne-Catherine Dolens, Kaat Durinck, Katrien De Mulder, Wouter Van Loocke, Sagar Damle, Els Waegemans, et al. 2016. “GATA3 Induces Human T-cell Commitment by Restraining Notch Activity and Repressing NK-cell Fate.” Nature Communications 7.
APA
Van de Walle, I., Dolens, A.-C., Durinck, K., De Mulder, K., Van Loocke, W., Damle, S., Waegemans, E., et al. (2016). GATA3 induces human T-cell commitment by restraining Notch activity and repressing NK-cell fate. NATURE COMMUNICATIONS, 7.
Vancouver
1.
Van de Walle I, Dolens A-C, Durinck K, De Mulder K, Van Loocke W, Damle S, et al. GATA3 induces human T-cell commitment by restraining Notch activity and repressing NK-cell fate. NATURE COMMUNICATIONS. 2016;7.
MLA
Van de Walle, Inge, Anne-Catherine Dolens, Kaat Durinck, et al. “GATA3 Induces Human T-cell Commitment by Restraining Notch Activity and Repressing NK-cell Fate.” NATURE COMMUNICATIONS 7 (2016): n. pag. Print.