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Updated: Nov 7, 2025

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
Published on: May 17, 2016
Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler
Chase M Woodley1, Alexander S Romer2, Jing Wang3,4
1Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Abstract:
The SNF5 subunit of the SWI/SNF chromatin remodeling complex has been shown to act as a tumor suppressor through multiple mechanisms, including impairing the ability of the oncoprotein transcription factor MYC to bind chromatin. Beyond SNF5, however, it is unknown to what extent MYC can access additional SWI/SNF subunits or how these interactions affect the ability of MYC to drive transcription, particularly in SNF5-null cancers. Here, we report that MYC interacts with multiple SWI/SNF components independent of SNF5. We show that MYC binds the pan-SWI/SNF subunit BAF155 through the BAF155 SWIRM domain, an interaction that is inhibited by the presence of SNF5. In SNF5-null cells, MYC binds with remaining SWI/SNF components to essential genes, although for a purpose that is distinct from chromatin remodeling. Analysis of MYC-SWI/SNF target genes in SNF5-null cells reveals that they are associated with core biological functions of MYC linked to protein synthesis. These data reveal that MYC can bind SWI/SNF in an SNF5-independent manner and that SNF5 modulates access of MYC to core SWI/SNF complexes. This work provides a framework in which to interrogate the influence of SWI/SNF on MYC function in cancers in which SWI/SNF or MYC are altered.
Insights
MYC oncoprotein interacts with SWI/SNF components independently of SNF5, impacting gene transcription in SNF5-null cancers. SNF5 modulates MYC
Area of Science:
- * Molecular Biology
- * Cancer Biology
- * Epigenetics
Background:
- * The SNF5 subunit of the SWI/SNF complex suppresses tumors by inhibiting MYC binding to chromatin.
- * The interaction of MYC with other SWI/SNF subunits and its impact on transcription in SNF5-null cancers remain largely unexplored.
Purpose of the Study:
- * To investigate MYC interactions with SWI/SNF subunits independent of SNF5.
- * To determine how these interactions affect MYC's transcriptional activity in SNF5-null cancers.
- * To elucidate the role of SWI/SNF in MYC-driven transcription in the context of altered SWI/SNF or MYC.
Main Methods:
- * Co-immunoprecipitation assays to detect MYC-SWI/SNF subunit interactions.
- * Chromatin immunoprecipitation sequencing (ChIP-seq) to identify MYC and SWI/SNF binding sites on genes.
- * Gene expression analysis to assess the functional consequences of MYC-SWI/SNF interactions.
Main Results:
- * MYC interacts with multiple SWI/SNF components, including BAF155, independently of SNF5.
- * SNF5 inhibits the binding of MYC to the BAF155 SWIRM domain.
- * In SNF5-null cells, MYC binds SWI/SNF components to essential genes involved in protein synthesis, distinct from canonical chromatin remodeling functions.
Conclusions:
- * MYC can associate with SWI/SNF complexes in an SNF5-independent manner.
- * SNF5 acts as a modulator of MYC's access to core SWI/SNF complexes.
- * This study provides a foundation for understanding SWI/SNF's influence on MYC function in cancers with SWI/SNF or MYC alterations.
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