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bioRxiv · 10.1101/013904

Mbd3 and deterministic reprogramming

Paul Bertone·Brian Hendrich·José C.R. Silva
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Abstract

Embryonic development requires the activity of the Nucleosome Remodeling and Deacetylase (NuRD) complex. NuRD functionality can be ablated by rendering cells devoid of methyl-CpG-binding domain protein 3 (Mbd3), a critical component that confers stability to the complex1. Previous studies noted that Mbd3-/- embryonic stem (ES) cells misregulate a subset of pluripotency-associated genes, and subsequently fail to engage in cell differentiation into embryonic lineages when self-renewal requisites (e.g. LIF) are withdrawn from culture media2-3. Components of the NuRD complex have been shown to interact with Oct4 and Nanog, two important transcription factors operative in the production of iPS cells4-7. Thus, elucidating the role of Mbd3/NuRD in the reprogramming process is of relevance to the field.\n\nRais et al. reported the remarkable obse ...

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Paul Bertone, Brian Hendrich, José C.R. Silva. 2015-01-16. Mbd3 and deterministic reprogramming. https://doi.org/10.1101/013904

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