Transcription factor overexpression increases binding at physiologically bound sites rather than creating new binding sites with distinct characteristics.
Preserves MyoD binding specificity upon overexpression; leaves open translation to human cardiac muscle regeneration.
BACKGROUND: Transcription factor overexpression is common in biological experiments and transcription factor amplification is associated with many cancers, yet few studies have directly compared the DNA-binding profiles of endogenous versus overexpressed transcription factors. METHODS: We analyzed MyoD ChIP-seq data from C2C12 mouse myotubes, primary mouse myotubes, and mouse fibroblasts differentiated into muscle cells by overexpression of MyoD and compared the genome-wide binding profiles and binding site characteristics of endogenous and overexpressed MyoD. RESULTS: Overexpressed MyoD bound to the same sites occupied by endogenous MyoD and possessed the same E-box sequence preference and co-factor site enrichments, and did not bind to new sites with distinct characteristics. CONCLUSIONS: Our data demonstrate a robust fidelity of transcription factor binding sites over a range of expression levels and that increased amounts of transcription factor increase the binding at physiologically bound sites.
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Yao et al. (2013) studied this question.
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