During development and differentiation, the expression of banscription factors is regulated in a temporal fashion. Newly expressed transcription factors must interact productively with target genes organized in chromatin. Although the mechanisms governing factor binding to chromatin templates are not well understood, it is now clear that template access can be dramatically influenced by nudeoprotein structure. We have examined the ability of a well characterized ranwactivator, the progesterone receptor (PR), to activate the mouse mammna tumor virus (MMTV) promoter organized either in stable, replicating templates that have a highly ordered nucleosome structure or as transiently transfected DNA, which adopts a less-dermed structure. (8). In this structural configuration, nuclear factor 1 (NF1) is excluded from its target site in the proximal promoter (1, 6, 9, 10). Binding of the activated glucocorticoid receptor (GR) to the promoter induces a chromatin remodeling event associated with the second nucleosome (Nuc-B) (8, 11). In addition, histone Hi is depleted from the promoter proximal region in a hormone-dependent manner (12). We proposed previously that this chromatin transition is directly and mechanistically involved in the binding of NF1 and subsequent formation of the transcription preinitiation complex (9, 10). Similar phenomena have been observed for the murine tyrosine aminotransferase (13-15) and yeast phoS (2,16) genes.The progesterone receptor (PR) and GR activate the MMTV promoter through the same target sequences as determined by transient transfections (17)(18)(19)(20)

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HTLV-II has been associated with a variety of lymphoproliferative disorders, including atypical hairy cell leukemia, chronic T cell leukemia, T prolymphocytic leukemia, and large granular lymphocytic leukemia. However, a direct or indirect role for HTLV-II in these disorders is not yet firmly established. We studied a patient diagnosed as having leukemia of the large granular lymphocyte (LGL) type who was HTLV-II seropositive, to determine if the expanded cell population was infected. Two populations of CD3-CD16+ LGL were identified; one was CD8+, the other CD8-. Populations of cells with these surface markers as well as normal CD3+CD4+ and CD3+CD8+ cells were separated by flow cytometric methods, DNA extracted, and gene regions of HTLV-II pol and tax amplified, using the polymerase chain reaction, and probed after Southern blotting. HTLV-II was detected in the CD3+CD8+ population, and not in the CD3-CD16+ large granular lymphocyte population. This finding indicates that the role of HTLV-II, if any, in LGL proliferation is indirect.

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