Research Papers:

C-Jun recruits the NSL complex to regulate its target gene expression by modulating H4K16 acetylation and promoting the release of the repressive NuRD complex

Yan Liu, Yuehong Long, Zhaobin Xing and Daoyong Zhang _

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Oncotarget. 2015; 6:14497-14506. https://doi.org/10.18632/oncotarget.3988

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Yan Liu1, Yuehong Long1, Zhaobin Xing1 and Daoyong Zhang2

1 College of Life Sciences, Hebei United University, Tangshan, China

2 Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA, USA

Correspondence to:

Daoyong Zhang, email:

Keywords: C-Jun; NSL complex; H4K16 acetylation; NuRD complex; phosphorylation

Received: March 04, 2015 Accepted: April 15, 2015 Published: May 04, 2015


The proto-oncogene c-Jun plays essential roles in various cellular processes, including cell proliferation, cell differentiation, and cellular apoptosis. Enormous efforts have been made to understand the mechanisms regulating c-Jun activation. The males absent on the first (MOF)-containing non-specific lethal (NSL) complex has been shown to positively regulate gene expression. However, the biological function of the NSL complex is largely unknown. Here we present evidence showing that c-Jun recruits the NSL complex to c-Jun target genes upon activation. The NSL complex catalyzes H4K16 acetylation at c-Jun target genes, thereby promoting c-Jun target gene transcription. More interestingly, we also found that the NSL complex promotes the release of the repressive NuRD complex from c-Jun target genes, thus activating c-Jun. Our findings not only reveal a new mechanism regulating c-Jun activation, but also identify the NSL complex as a c-Jun co-activator in c-Jun-regulated gene expression, expanding our knowledge of the function of the NSL complex in gene expression regulation.

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