Is REST a regulator of pluripotency?

Noel J. Buckley, Rory Johnson, Yuh-Man Sun and Lawrence W. Stanton
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Noel J. Buckley: * King’s College London, Institute of Psychiatry, Centre for the Cellular Basis of Behaviour, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK. noel.buckley@iop.kcl.ac.uk
Rory Johnson: † Stem Cell and Developmental Biology, Genome Institute of Singapore, 60 Biopolis Street #02-01, Genome Building, Singapore 138672
Yuh-Man Sun: * King’s College London, Institute of Psychiatry, Centre for the Cellular Basis of Behaviour, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK. noel.buckley@iop.kcl.ac.uk
Lawrence W. Stanton: † Stem Cell and Developmental Biology, Genome Institute of Singapore, 60 Biopolis Street #02-01, Genome Building, Singapore 138672

Nature, 2009, vol. 457, issue 7233, E5-E6

Abstract: Abstract Arising from: S. K. Singh, M. N. Kagalwala, J. Parker-Thornburg, H. Adams & S. Majumder Nature 453, 223–227 (2008)10.1038/nature06863 ; Singh et al. reply Establishment and maintenance of the pluripotent state of ESCs is a key issue in stem cell biology and regenerative medicine, and consequently identification of transcription factors that regulate ESC pluripotency is an important goal. Singh et al.1 claim that the transcriptional repressor REST is such a regulator and that a 50% reduction of REST in ESCs leads to activation of a specific microRNA, miR-21, and that this subsequently results in loss of pluripotency markers and a reciprocal gain in some lineage-specific differentiation markers. In contrast, we show that, in haplodeficient Rest+/- ESCs, we detected no change in pluripotency markers, no precocious expression of differentiated neuronal markers and no interaction of REST with miR-21. It is vital that identification of factors that regulate pluripotency is based on robust, consistent data, and the contrast in data reported here undermines the claim by Singh et al.1 that REST is such a regulator.

Date: 2009
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DOI: 10.1038/nature07784

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