Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

A novel genetic strategy reveals unexpected roles of the Swi-Snf-like chromatin-remodeling BAF complex in thymocyte development.

We have developed a general strategy for creating littermates bearing either a tissue-specific point mutation or deletion in any target gene, and used the method to dissect the roles of Brg, the ATPase subunit of the chromatin-remodeling Brg-associated factor (BAF) complex, in early thymocyte development. We found that a point mutation that inactivates the Brg ATPase recapitulates multiple defects previously described for Brg deletion (Chi, T.H., M. Wan, P.P. Lee, K. Akashi, D. Metzger, P. Chambon, C.B. Wilson, and G.R. Crabtree. 2003. Immunity. 19:169-182). However, the point mutant helps reveal unexpected roles of Brg in CD25 repression and CD4 activation. Surprisingly, CD4 activation occurs independently of the Brg ATPase and is perhaps mediated by physical interactions between Brg and the CD4 locus. Our study thus suggests that the BAF complex harbors novel activities that can be necessary and even sufficient for stimulating transcription from an endogenous chromatin template in the absence of Brg-dependent remodeling of that template. We conclude that conditional point mutants, rarely used in mammalian genetics, can help uncover important gene functions undetectable or overlooked in deletion mutants.

Pubmed ID: 18955569


  • Jani A
  • Wan M
  • Zhang J
  • Cui K
  • Wu J
  • Preston-Hurlburt P
  • Khatri R
  • Zhao K
  • Chi T


The Journal of experimental medicine

Publication Data

November 24, 2008

Associated Grants

  • Agency: NIAID NIH HHS, Id: R01AI063554-02
  • Agency: Intramural NIH HHS, Id:

Mesh Terms

  • Animals
  • Antigens, CD4
  • Chromatin
  • Chromosomal Proteins, Non-Histone
  • DNA Helicases
  • Gene Deletion
  • Gene Expression Regulation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Nuclear Proteins
  • Phenotype
  • Point Mutation
  • T-Lymphocytes
  • Thymus Gland
  • Transcription Factors
  • Transcription, Genetic
  • bcl-X Protein