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Acetylation reprograms MITF target selectivity and residence time

Abstract:
The ability of transcription factors to discriminate between different classes of binding sites associated with specific biological functions underpins effective gene regulation in development and homeostasis. How this is achieved is poorly understood. The microphthalmia-associated transcription factor MITF is a lineage-survival oncogene that plays a crucial role in melanocyte development and melanoma. MITF suppresses invasion, reprograms metabolism and promotes both proliferation and differentiation. How MITF distinguishes between differentiation and proliferation-associated targets is unknown. Here we show that compared to many transcription factors MITF exhibits a very long residence time which is reduced by p300/CBP-mediated MITF acetylation at K206. While K206 acetylation also decreases genome-wide MITF DNA-binding affinity, it preferentially directs DNA binding away from differentiation-associated CATGTG motifs toward CACGTG elements. The results reveal an acetylation-mediated switch that suppresses differentiation and provides a mechanistic explanation of why a human K206Q MITF mutation is associated with Waardenburg syndrome.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-023-41793-7

Authors


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Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
ORCID:
0000-0001-6546-332X
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Role:
Author
ORCID:
0000-0003-4523-5666
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Role:
Author
ORCID:
0000-0002-1021-6804


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
14
Article number:
6051
Publication date:
2023-09-28
Acceptance date:
2023-09-08
DOI:
EISSN:
2041-1723
Pmid:
37770430


Language:
English
Keywords:
Pubs id:
1537577
Local pid:
pubs:1537577
Deposit date:
2023-10-11

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