Lipids alter the level and distribution of mouse mammary tumor virus gp52 in vitro

Sunzeri, Franklin J.; Buehring, Gertrude Case

doi:10.1016/0304-3835(93)90044-a

Cited by 1 publication

(1 citation statement)

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“…Deletion of one or more NREs leads to increased MMTV expression in non-permissive tissues as well as cell lines derived from semipermissive tissues (6,11,12). In addition, MMTV strains that lack the NREs induce primarily T-cell lymphomas rather than breast cancer (8), yet mammotropic strains require replication in B and T cells for transmission to mammary cells (13)(14)(15)(16)(17)(18). Because of the limited coding capacity of MMTV and other retroviruses (19), negative regulation of viral transcription must be controlled by cellular proteins.…”

Section: Mouse Mammary Tumor Virus (Mmtv)mentioning

confidence: 99%

Nuclear Matrix Binding Regulates SATB1-mediated Transcriptional Repression

Seo

Lozano

Dudley

2005

Journal of Biological Chemistry

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Special AT-rich binding protein 1 (SATB1) originally was identified as a protein that bound to the nuclear matrix attachment regions (MARs) of the immunoglobulin heavy chain intronic enhancer. Subsequently, SATB1 was shown to repress many genes expressed in the thymus, including interleukin-2 receptor ␣, c-myc, and those encoded by mouse mammary tumor virus (MMTV), a glucocorticoid-responsive retrovirus. SATB1 binds to MARs within the MMTV provirus to repress transcription. To address the role of the nuclear matrix in SATB1-mediated repression, a series of SATB1 deletion constructs was used to determine protein localization. Wild-type SATB1 localized to the soluble nuclear, chromatin, and nuclear matrix fractions. Mutants lacking amino acids 224 -278 had a greatly diminished localization to the nuclear matrix, suggesting the presence of a nuclear matrix targeting sequence (NMTS). Transient transfection experiments showed that NMTS fusions to green fluorescent protein or LexA relocalized these proteins to the nuclear matrix. Difficulties with previous assay systems prompted us to develop retroviral vectors to assess effects of different SATB1 domains on expression of MMTV proviruses or integrated reporter genes. SATB1 overexpression repressed MMTV transcription in the presence and absence of functional glucocorticoid receptor. Repression was alleviated by deletion of the NMTS, which did not affect DNA binding, or by deletion of the MAR-binding domain. Our studies indicate that both nuclear matrix association and DNA binding are required for optimal SATB1-mediated repression of the integrated MMTV promoter and may allow insulation from cellular regulatory elements.

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