Regulation of expression driven by human immunodeficiency virus type 1 and human T-cell leukemia virus type I long terminal repeats in pluripotential human embryonic cells

Journal Article · Fri Apr 01 04:00:00 EST 1988 · Journal of Virology; (USA)

OSTI ID:6522768

Maio, J; Brown, F L ^[1]

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1. Albert Einstein College of Medicine, Bronx, NY (USA)

Human pluripotential embryonic teratocarcinoma cells differentially expressed gene activity controlled by the human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus type I (HTLV-I) long terminal repeats (LTRs) when differentiation was induced by the morphogen all-trans retinoic acid. The alterations occurred after commitment and before the appearance of the multiple cell types characteristic of these pluripotential cells. After commitment, gene activity controlled by the HIV-1 LTR markedly increased, whereas that controlled by the HTLV-I LTR decreased. Steady-state mRNA levels and nuclear run-on transcription indicated that the increased HIV-1-directed activity during differentiation occurred posttranscriptionally, whereas the decreased HTLV-I activity was at the transcriptional level. Phorbol esters did not cause commitment but strongly enhanced expression by both viral LTRs at the transcriptional level. Differentiating cells gradually lost the ability to respond to phorbol ester stimulation. Experiments with a deletion mutant of the HIV-1 LTR suggested that this was due to imposition of negative regulation during differentiation that was not reversed by phorbol ester induction. Cycloheximide, with or without phorbol ester, slightly stimulated HIV-1-directed activity at the transcriptional level and massively increased the amounts of steady-state mRNA by posttranscriptional superinduction. It appeared, however, that new nuclear protein synthesis was required for maximal transcriptional stimulation by phorbol esters. Thus, changing cellular regulatory mechanisms influenced human retrovirus expression during human embryonic cell differentiation.

• OSTI ID: 6522768
• Journal Information: Journal of Virology; (USA), Journal Name: Journal of Virology; (USA) Vol. 62:4; ISSN 0022-538X; ISSN JOVIA
• Country of Publication: United States
• Language: English

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59 BASIC BIOLOGICAL SCIENCES
AIDS VIRUS
ANIMAL CELLS
ANIMALS
AUTORADIOGRAPHY
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BIOLOGICAL EFFECTS
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BODY FLUIDS
CARBOXYLIC ACID ESTERS
CARCINOGENS
CARCINOMAS
CELL DIFFERENTIATION
CONNECTIVE TISSUE CELLS
DAYS LIVING RADIOISOTOPES
DISEASES
EMBRYONIC CELLS
ESTERS
GENE REGULATION
ISOTOPES
LEUKEMIA VIRUSES
LEUKOCYTES
LIGHT NUCLEI
LYMPHOCYTES
MAMMALS
MAN
MATERIALS
MICROORGANISMS
NEOPLASMS
NUCLEI
ODD-ODD NUCLEI
ONCOGENIC VIRUSES
ORGANIC COMPOUNDS
PARASITES
PHORBOL ESTERS
PHOSPHORUS 32
PHOSPHORUS ISOTOPES
PRIMATES
RADIOISOTOPES
RETINOIC ACID
SOMATIC CELLS
TUMOR CELLS
VERTEBRATES
VIRUSES