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Splicing of a human endogenous retrovirus to a novel phospholipase A2 related gene

A E Feuchter-Murthy1, J D Freeman, D L Mager

  • 1Terry Fox Laboratory, B.C. Cancer Agency, Vancouver, Canada.

Nucleic Acids Research
|January 11, 1993
PubMed

Insights

Endogenous retroviruses can activate adjacent genes. Researchers found a novel human gene, PLA2L, fused with a retroviral element (RTVL-H) in teratocarcinoma cells, suggesting LTR-driven gene expression.

Area of Science:

  • Genomics
  • Molecular Biology
  • Retroviral Studies

Background:

  • Endogenous retroviruses (ERVs) are remnants of ancient viral infections integrated into host genomes.
  • The impact of ERVs on the regulation of adjacent cellular genes is an area of ongoing research.
  • Teratocarcinoma cells offer a unique model for studying gene expression and differentiation.

Purpose of the Study:

  • To investigate the effects of endogenous retroviruses on adjacent gene expression.
  • To characterize a novel chimeric transcript involving an ERV and a cellular gene.
  • To determine the role of the RTVL-H long terminal repeat (LTR) in gene activation.

Main Methods:

  • cDNA cloning and sequencing from NTera2D1 teratocarcinoma cells.
  • Southern blot analysis to determine gene structure and copy number.
  • Polymerase Chain Reaction (PCR) to detect and analyze alternative splicing.
  • Transcriptional analysis to identify promoter usage.

Main Results:

  • A chimeric cDNA clone (AF-5) was isolated, representing a fusion of RTVL-H and downstream cellular sequences.
  • AF-5 contains an open reading frame with homology to phospholipase A2 (PLA2), defining a novel gene PLA2L.
  • RTVL-H/PLA2L chimeric transcripts were specifically detected in teratocarcinoma cell lines, not in other tissues.
  • Alternative splicing of RTVL-H/PLA2L transcripts was observed, with no evidence of non-LTR promoter activity.

Conclusions:

  • The RTVL-H long terminal repeat (LTR) acts as a promoter for the human PLA2L gene in teratocarcinoma cells.
  • This study reveals a novel mechanism of gene regulation mediated by endogenous retroelements.
  • The findings highlight the potential role of ERVs in shaping gene expression patterns during cellular differentiation or disease states.

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