Bright/Arid3A acts as a barrier to somatic cell reprogramming through direct regulation of Oct4, Sox2, and Nanog

Melissa Popowski, Troy D. Templeton, Bum Kyu Lee, Catherine Rhee, He Li, Cathrine Miner, Joseph D. Dekker, Shari Orlanski, Yehudit Bergman, Vishwanath R. Iyer, Carol F. Webb, Haley Tucker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


We show here that singular loss of the Bright/Arid3A transcription factor leads to reprograming of mouse embryonic fibroblasts (MEFs) and enhancement of standard four-factor (4F) reprogramming. Bright-deficient MEFs bypass senescence and, under standard embryonic stem cell (ESC) culture conditions, spontaneously form clones that in vitro express pluripotency markers, differentiate to all germ lineages, and in vivo form teratomas and chimeric mice. We demonstrate that BRIGHT binds directly to the promoter/enhancer regions of Oct4, Sox2, and Nanog to contribute to their repression in both MEFs and ESCs. Thus, elimination of the BRIGHT barrier may provide an approach for somatic cell reprogramming.

Original languageAmerican English
Pages (from-to)26-35
Number of pages10
JournalStem Cell Reports
Issue number1
StatePublished - 14 Jan 2014

Bibliographical note

Funding Information:
This work was funded by grants from the NIH (CA-31534, NHARP-003658-0149), Cancer Prevention Research Institute (CPRIT RP100612), and the Maria Betzner Morrow Endowment to H.T. and by an Oklahoma Center for Adult Stem Cell Research award to C.F.W. M.P. is a CPRIT scholar (CPRIT RP101501). We thank Chhaya Das, June Harriss, Maya Ghosh, Amrita Das, Charles Martin, Hongxia Liu, and Stephen Chiang for technical assistance and Jonghwan Kim for discussion and critical reading of the manuscript. We thank the CPRIT Core Facility Support group (CPRIT-RP120348) for assistance with ChIP sequencing library and sequencing.


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