Transcription factor GATA-3 regulates the transcriptional activity of dopamine β-hydroxylase by interacting with Sp1 and AP4

Seok Jong Hong; Hyun Jin Choi; Sunghoi Hong; Youngbuhm Huh; Han Chae; Kwang Soo Kim

doi:10.1007/s11064-008-9639-3

Transcription factor GATA-3 regulates the transcriptional activity of dopamine β-hydroxylase by interacting with Sp1 and AP4

Seok Jong Hong
, Hyun Jin Choi
, Sunghoi Hong
, Youngbuhm Huh
, Han Chae
, Kwang Soo Kim^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

25 Citations (Scopus)

Abstract

GATA-3 is a zinc finger transcription factor that is expressed in T cell lineages as well as in the nervous system during development. In this study, we report that forced expression of GATA-3 resulted in an increased number of dopamine β-hydroxylase (DBH)-expressing neurons in primary neural crest stem cell (NCSC) culture, suggesting that the DBH gene may be a downstream target gene of GATA-3. GATA-3 robustly transactivates the promoter function of the noradrenaline (NA)-synthesizing DBH gene, via two specific upstream promoter domains; one at -62 to -32 bp and the other at -891 to -853 bp. Surprisingly, none of these domains contain GATA-3 binding sites but encompass binding motifs for transcription factors Sp1 and AP4, respectively. Protein-protein interaction analyses both in vitro and in vivo and chromatin immunoprecipitation (ChIP) assays showed that GATA-3 effects its transcriptional regulatory function through physical interactions with these transcription factors.

Original language	English
Pages (from-to)	1821-1831
Number of pages	11
Journal	Neurochemical Research
Volume	33
Issue number	9
DOIs	https://doi.org/10.1007/s11064-008-9639-3
Publication status	Published - 2008 Sept
Externally published	Yes

Bibliographical note

Funding Information:
Acknowledgements The authors thank J. Engel for chick GATA-3 clone, R. Ratan for the Sp1 expressing plasmids, C. Tabin for RCASBP vectors and pSlax13, and O. Andrisani for NCSC culture. This work was supported by NIH grants (MH48866 and DC006501).

Keywords

AP4
ChIP assay
Dopamine β-hydroxylase
GATA-3
Protein-protein interaction
Sp1
siRNA

ASJC Scopus subject areas

Biochemistry
Cellular and Molecular Neuroscience

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10.1007/s11064-008-9639-3

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title = "Transcription factor GATA-3 regulates the transcriptional activity of dopamine β-hydroxylase by interacting with Sp1 and AP4",

abstract = "GATA-3 is a zinc finger transcription factor that is expressed in T cell lineages as well as in the nervous system during development. In this study, we report that forced expression of GATA-3 resulted in an increased number of dopamine β-hydroxylase (DBH)-expressing neurons in primary neural crest stem cell (NCSC) culture, suggesting that the DBH gene may be a downstream target gene of GATA-3. GATA-3 robustly transactivates the promoter function of the noradrenaline (NA)-synthesizing DBH gene, via two specific upstream promoter domains; one at -62 to -32 bp and the other at -891 to -853 bp. Surprisingly, none of these domains contain GATA-3 binding sites but encompass binding motifs for transcription factors Sp1 and AP4, respectively. Protein-protein interaction analyses both in vitro and in vivo and chromatin immunoprecipitation (ChIP) assays showed that GATA-3 effects its transcriptional regulatory function through physical interactions with these transcription factors.",

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note = "Funding Information: Acknowledgements The authors thank J. Engel for chick GATA-3 clone, R. Ratan for the Sp1 expressing plasmids, C. Tabin for RCASBP vectors and pSlax13, and O. Andrisani for NCSC culture. This work was supported by NIH grants (MH48866 and DC006501).",

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AU - Hong, Sunghoi

AU - Huh, Youngbuhm

AU - Chae, Han

AU - Kim, Kwang Soo

N1 - Funding Information: Acknowledgements The authors thank J. Engel for chick GATA-3 clone, R. Ratan for the Sp1 expressing plasmids, C. Tabin for RCASBP vectors and pSlax13, and O. Andrisani for NCSC culture. This work was supported by NIH grants (MH48866 and DC006501).

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N2 - GATA-3 is a zinc finger transcription factor that is expressed in T cell lineages as well as in the nervous system during development. In this study, we report that forced expression of GATA-3 resulted in an increased number of dopamine β-hydroxylase (DBH)-expressing neurons in primary neural crest stem cell (NCSC) culture, suggesting that the DBH gene may be a downstream target gene of GATA-3. GATA-3 robustly transactivates the promoter function of the noradrenaline (NA)-synthesizing DBH gene, via two specific upstream promoter domains; one at -62 to -32 bp and the other at -891 to -853 bp. Surprisingly, none of these domains contain GATA-3 binding sites but encompass binding motifs for transcription factors Sp1 and AP4, respectively. Protein-protein interaction analyses both in vitro and in vivo and chromatin immunoprecipitation (ChIP) assays showed that GATA-3 effects its transcriptional regulatory function through physical interactions with these transcription factors.

AB - GATA-3 is a zinc finger transcription factor that is expressed in T cell lineages as well as in the nervous system during development. In this study, we report that forced expression of GATA-3 resulted in an increased number of dopamine β-hydroxylase (DBH)-expressing neurons in primary neural crest stem cell (NCSC) culture, suggesting that the DBH gene may be a downstream target gene of GATA-3. GATA-3 robustly transactivates the promoter function of the noradrenaline (NA)-synthesizing DBH gene, via two specific upstream promoter domains; one at -62 to -32 bp and the other at -891 to -853 bp. Surprisingly, none of these domains contain GATA-3 binding sites but encompass binding motifs for transcription factors Sp1 and AP4, respectively. Protein-protein interaction analyses both in vitro and in vivo and chromatin immunoprecipitation (ChIP) assays showed that GATA-3 effects its transcriptional regulatory function through physical interactions with these transcription factors.

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Transcription factor GATA-3 regulates the transcriptional activity of dopamine β-hydroxylase by interacting with Sp1 and AP4

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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