Open Access
Enhancer sequences of a retroviral vector determine expression of a gene in multipotent hematopoietic progenitors and committed erythroid cells.
Author(s) -
Christie A. Holland,
Pervin Anklesaria,
Mary Ann Sakakeeny,
Joel S. Greenberger
Publication year - 1987
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.84.23.8662
Subject(s) - biology , enhancer , progenitor cell , haematopoiesis , microbiology and biotechnology , murine leukemia virus , viral vector , transfection , cell culture , virology , virus , genetic enhancement , stem cell , gene , gene expression , genetics , recombinant dna
To analyze the transcriptional activity of retroviral enhancer sequences in hematopoietic lineages, we determined the effect of enhancer sequences on the expression of the neomycin resistance gene transferred by two retroviral vectors to primary hematopoietic lineages. We constructed the vector pFr-SV(X). The Moloney murine leukemia virus enhancer region of a vector, pZIP-SV(X), was replaced by a 380-nucleotide-long fragment containing the enhancer sequences of the Friend murine leukemia virus. The enhancer sequences of Friend murine leukemia virus were used because these sequences have been shown to target the disease specificity of the virus to the erythroid lineage. Hematopoietic progenitors in murine continuous marrow cultures were infected with identical numbers of pure defective, infectious viral vector particles of either pFr-SV(X) or pZIP-SV(X). Expression of the transferred neomycin resistance gene in multipotential stem cells and their differentiated progeny was assayed as the ability of infected progenitors to form colonies (greater than 50 cells) in G418. Expression of the neomycin resistance gene in multipotential progenitor cells during the entire 11 weeks of the cultures was independent of the vector used to transfer the gene. Conversely, committed hemoglobinized erythroid bursts and myeloid colonies resistant to G418 were consistently produced by pFr-SV(X)-infected cultures but not pZIP-SV(X)-infected cultures. These results demonstrate that both pFr-SV(X) and pZIP-SV(X) were stably integrated and expressed in more primitive, multilineage, hematopoietic progenitor cells and suggest that the enhancer sequences of a vector affects expression of the transferred neomycin resistance gene when these cells differentiate to committed myeloid and erythroid cells.