Submitted June 20, 2006
Accepted October 12, 2006
Transcriptional interference among the murine 
-like globin genes
Xiao Hu, Susan Eszterhas, Nicholas Pallazzi, Eric E Bouhassira, Jennifer Fields, Osamu Tanabe, Scott A Gerber, Michael Bulger, James Douglas Engel, Mark Groudine, and Steven Fiering*
Dept of Microbiology/Immunology & Norris Cotton Cancer Centr, Dartmouth Medical School, Hanover, NH
Dept of Medicine, Division of Hematology, Albert Einstein College of Medicine, Bronx, NY
Dept of Cell & Developmental Biology, University of Michigan Medical School, Ann Arbor, MI
Dept of Genetics & Norris Cotton Cancer Center, Dartmouth Medical School, Hanover, NH
Center for Human Genetics & Molecular Pediatrics, University of Rochester Medical School, Rochester, NY
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA
* Corresponding author; email: fiering{at}dartmouth.edu.
Mammalian 
-globin loci contain multiple genes that are activated at different development stages. Studies have suggested that transcription of one gene in the locus can influence expression of the other locus genes. The prevalent model to explain this transcriptional interference is that all potentially active genes compete for LCR activity. To investigate the influence of transcription by the murine embryonic genes on transcription of the other -like genes, we generated mice with deletions of the promoter regions of Ey and h1, and measured transcription of the remaining genes. Deletion of the Ey and h1 promoters, increased transcription of major and minor 2- to 3-fold during primitive erythropoiesis. Deletion of Ey did not affect h1 and vice versa, but Ey deletion uniquely activated transcription from h0, a -like globin gene immediately downstream of Ey. Protein analysis shows that h0 encodes a translatable -like globin protein that can pair with alpha globin. The lack of transcriptional interference between Ey and h1 and the gene-specific repression of h0 does not support LCR competition among the embryonic genes and suggests that direct transcriptional interference from Ey, suppresses h0.
