PU.1 as a chromatin accessibility factor for immunoglobulin genes

Sylvia Marecki, Kevin M. McCarthy, Barbara S. Nikolajczyk

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


The hematopoietic-specific transcription factor PU.1 is a chromatin accessibility factor, based on analysis of the immunoglobulin heavy chain intronic (μ) enhancer. Whether PU.1 functions as an accessibility factor for additional PU.1-regulated genes is unknown. Outside the constraints of chromatin, PU.1 binds and activates transcription through both μ and κ3′ immunoglobulin enhancers, among others. The DNA-binding ETS domain of PU.1 is sufficient for activating both enhancers in an extrachromosomal context. New data show that the ETS domain of PU.1 is sufficient for increasing accessibility of a closed μ enhancer chromatin structure proximal to the PU.1-binding site. In contrast, PU.1 does not alter widespread chromatin accessibility. Furthermore, PU.1 does not induce accessibility proximal or distal to its binding site on the κ3′ enhancer. Taken together the data demonstrate that PU.1 induces chromatin accessibility proximal to its binding site at a locus activated early in development, the μ locus. PU.1 does not function as an accessibility factor for the κ3′ enhancer, which regulates a locus important for later stages of B cell development. We conclude that PU.1 is a context-dependent chromatin accessibility factor that, alone, cannot establish widespread accessibility required for critical developmental processes such as antigen receptor recombination.

Original languageEnglish
Pages (from-to)723-731
Number of pages9
JournalMolecular Immunology
Issue number10
StatePublished - Jan 2004

Bibliographical note

Funding Information:
The authors appreciate PU.1 deletion constructs generated by Dr. Batu Erman. The technical expertise of Amy Andreucci has been invaluable. Critical comments on the manuscript have been graciously supplied by Dr. Ranjan Sen. This work was supported by R01 AI54611, The Evans Medical Foundation, and an Arthritis Foundation Biomedical Sciences Grant to B.N. K.M. was supported by NIH Training Grant T32-CA64070.


  • B lymphocytes
  • Chromatin accessibility
  • Gene regulation
  • PU.1
  • Transcription factors

ASJC Scopus subject areas

  • Immunology
  • Molecular Biology


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