Transcription of the hypersensitive site HS2 enhancer in erythroid cells

Dorothy Tuan, Suming Kong, Kenneth Hu

Research output: Contribution to journalArticlepeer-review

159 Scopus citations


In the human genome, the erythroid-specific hypersensitive site HS2 enhancer regulates the transcription of the downstream β-like globin genes 10-50 kilobases away. The mechanism of HS2 enhancer function is not known. The present study employs RNA protection assays to analyze the transcriptional status of the HS2 enhancer in transfected recombinant chloramphenicol acetyltransferase (CAT) plasmids. In erythroid K562 cells in which the HS2 enhancer is active, the HS2 sequence directs the synthesis of long enhancer transcripts that are initiated apparently from within the enhancer and elongated through the intervening DNA into the cis-linked CAT gene. In nonerythroid HL-60 cells in which the HS2 enhancer is inactive, long enhancer transcripts are not detectable. Splitting the HS2 enhancer between two tandem Ap1 sites abolishes the synthesis of a group of long enhancer transcripts and results in loss of enhancer function and transcriptional silencing of the cis-linked CAT gene. In directing the synthesis of RNA through the intervening DNA and the gene by a tracking and transcription mechanism, the HS2 enhancer may (i) open up the chromatin structure of a gene domain and (ii) deliver enhancer binding proteins to the promoter sequence where they may stimulate the transcription of the gene at the cap site.

Original languageEnglish (US)
Pages (from-to)11219-11223
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number23
StatePublished - Dec 1 1992
Externally publishedYes


  • Ap1 sites
  • Enhancer function
  • Long enhancer transcripts
  • RNA protection assays

ASJC Scopus subject areas

  • General


Dive into the research topics of 'Transcription of the hypersensitive site HS2 enhancer in erythroid cells'. Together they form a unique fingerprint.

Cite this