Identification of a retinoic acid-inducible endogenous retroviral transcript in the human teratocarcinoma-derived

P Kannan1, R Buettner, D R Pratt

  • 1Department of Tumor Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.

Journal of Virology
|November 1, 1991
PubMed

Insights

Retinoic acid (RA) activates a novel human endogenous retrovirus (RRHERV-I) in PA-1 cells. This defective provirus, found in multiple copies in human DNA, represents the first RA-inducible human endogenous retroviral mRNA.

Area of Science:

  • Molecular Biology
  • Virology
  • Genetics

Background:

  • Retinoic acid (RA) is a crucial developmental morphogen.
  • Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections integrated into the host genome.
  • The transcriptional regulation of HERVs by developmental factors is not fully understood.

Purpose of the Study:

  • To investigate the effect of retinoic acid (RA) on endogenous retroviral elements in human cells.
  • To characterize a novel RA-responsive human endogenous retrovirus.

Main Methods:

  • RA treatment of human teratocarcinoma-derived PA-1 cells.
  • Analysis of retroviral transcript activation.
  • Determination of the nucleotide sequence of the viral cDNA.
  • Homology analysis with known HERV sequences.

Main Results:

  • RA induced the transcription of a defective endogenous retrovirus-related element in PA-1 cells.
  • This element, named RRHERV-I, exists as multicopy elements in human DNA.
  • The 3,357 bp cDNA sequence showed homology to ERV3 and 4-1 HERVs.
  • The cDNA contained characteristic retroviral sequences (R-U5-delta pol-env-U3-R) and a tRNA-binding site.

Conclusions:

  • RRHERV-I is the first identified human endogenous retroviral mRNA transcriptionally activated by RA.
  • RA-inducible HERVs may play a role in human development or cellular processes.
  • Further research into RRHERV-I function and regulation is warranted.

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