Loss of Bright/ARID3a function promotes developmental plasticity

Stem Cells. 2010 Sep;28(9):1560-7. doi: 10.1002/stem.491.


B-cell regulator of immunoglobulin heavy chain transcription (Bright)/ARID3a, an A+T-rich interaction domain protein, was originally discovered in B lymphocyte lineage cells. However, expression patterns and high lethality levels in knockout mice suggested that it had additional functions. Three independent lines of evidence show that functional inhibition of Bright results in increased developmental plasticity. Bright-deficient cells from two mouse models expressed a number of pluripotency-associated gene products, expanded indefinitely, and spontaneously differentiated into cells of multiple lineages. Furthermore, direct knockdown of human Bright resulted in colonies capable of expressing multiple lineage markers. These data suggest that repression of this single molecule confers adult somatic cells with new developmental options.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / metabolism
  • Cell Differentiation* / genetics
  • Cell Lineage* / genetics
  • Cell Proliferation*
  • Cells, Cultured
  • DNA-Binding Proteins / deficiency*
  • DNA-Binding Proteins / genetics
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Genes, Dominant
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Mice, Knockout
  • Mice, SCID
  • Mice, Transgenic
  • Pluripotent Stem Cells / metabolism*
  • RNA Interference
  • Teratoma / genetics
  • Teratoma / metabolism
  • Transcription Factors / deficiency*
  • Transcription Factors / genetics


  • ARID3A protein, human
  • Arid3a protein, mouse
  • Biomarkers
  • DNA-Binding Proteins
  • Transcription Factors