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. 2001 Sep 11;98(20):11450–11455. doi: 10.1073/pnas.201415498

Figure 1.

Figure 1

Lentiviral vectors and LV-Cre-mediated recombination in vitro and in vivo. (A) Schematic representation of the lentiviral vectors used in this study. (Top) The Cre lentiviral vector (LV-Cre) contains a Cre expression cassette with an nls. Expression of Cre is driven by the CMV promoter. (Middle) LV-CIG contains an internal ribosomal entry site (I) and a GFP cassette downstream of Cre. (Bottom) LV-Lac carries the lacZ gene instead of Cre. All vectors contain the Rous sarcoma virus promoter in the 5′ long-terminal repeat (LTR) (for efficient virus production in the context of a Tat-free packaging system), and self-inactivating mutations in the 3′ LTR (brown triangle). To enhance transgene expression in the target cells, a central ppt of HIV-1 pol (ppt) and a posttranscriptional element (W) from the woodchuck hepatitis virus were included. (B) Structure of the Cre-responsive lacZ reporter gene unit of CV-1 cells. Before Cre-mediated recombination, transcription from the CMV-β-actin promoter (thin black arrow) stops at the polyadenylation site of the neomycin resistance (neo) cassette. After recombination of the loxP sites (bold black arrows), this cassette is excised and the lacZ reporter gene is transcribed. Wavy line, chromosomal DNA. (C and D) X-gal stain of the CV-1 cells 72 h after infection with LV-Cre (moi ≈ 2) (C) and of uninfected CV-1 cells (D).