Activation of PU.1 in primary myeloblast clones induces DC phenotype. Clonal E26ts21-PUER virus (C-D, G-H, K-L, O-P)– or E26ts21 control virus (A-B, E-F, I-J, M-N)–transformed chicken myeloblasts were cultured for 48 hours either in the absence (-βE; A, C, E, G, I, K, M, O) or presence of 1 μM βE(+βE; B, D, F, H, J, L, N, P). (A-D) Phase contrast micrographs of cell cultures visualized under a Leica DMiL optical microscope equipped with a 40×/0.5 objective lens (Leica, Wetzlar, Germany). (E-H) May-Grünwald-Giemsa staining (MGG) of cytocentrifuged cells (shown at original magnification, ×40). (I-L) Immunofluorescence detection of MHCII with an FITC-conjugated secondary antibody. Images were viewed under a Leica DMRBE fluorescence microscope equipped with a 40×/1.0 objective lens (Leica) and a Nikon DVM1200 digital camera (Nikon, Champigny sur Marne, France). Lucia software version 4.61 was used for image processing (Nikon). (M-P) Immunofluorescence detection of S100 with an FITC-conjugated secondary antibody. Nuclei were counterstained with DAPI. (Q) Cells containing MHCII lysosomal vesicles (▪)or staining positive for S100 (▦) were counted for a total of at least 100 cells in 6 independent PUER clones cultured with or without βE.