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Reviving a 60 million year old LINE-1 element.

Bradley J Wagstaff1, Linda Wang1, Susan Lai1

  • 1Tulane Cancer Center SL-66, Dept. of Epidemiology, Tulane University Health Sciences Center, 1430 Tulane Ave., New Orleans, LA 70112.

Gene Reports
|September 18, 2018
PubMed
Summary
This summary is machine-generated.

Researchers revived an ancient LINE-1 (L1) retrotransposon, L1PA13A, finding its lower activity is due to both its proteins. Host cell environment influences L1 retrotransposition efficiency.

Keywords:
L1L1 familiesLINE-1ORF1 proteinORF2 proteinretrotransposition

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Area of Science:

  • Genetics
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Mobile genetic elements, particularly LINE-1 (L1) retrotransposons, have profoundly shaped genome evolution.
  • The human genome contains over half a million L1 copies, with most originating from ancient, extinct families.
  • Understanding the activity and constraints of ancient L1 elements provides insights into genome dynamics.

Purpose of the Study:

  • To reconstruct and functionally characterize the extinct L1PA13A retrotransposon, active approximately 60 million years ago.
  • To investigate the molecular basis for the reduced retrotransposition efficiency of L1PA13A compared to modern L1 elements.
  • To explore the influence of host cellular environments on L1 retrotransposition activity.

Main Methods:

  • Reconstruction of the extinct L1PA13A element using previously established methods.
  • Generation of chimeric L1 elements combining L1PA13A with modern L1PA1 and L1PA8 components (ORF1p and ORF2p).
  • Assays for retrotransposition efficiency in both human (HeLa) and rodent cell lines.
  • Functional analysis of L1PA13A ORF2p by assessing its ability to drive Alu retrotransposition.

Main Results:

  • The reconstructed L1PA13A is retrocompetent but exhibits significantly lower activity than L1PA1 and L1PA8 in human cells.
  • Both L1PA13A ORF1p and ORF2p contribute to the reduced retrotransposition efficiency.
  • In rodent cells, replacing L1PA13A ORF1p with L1PA1 ORF1p partially restores retrotransposition, indicating L1PA13A ORF2p is functional.
  • L1PA13A ORF2p successfully drives Alu retrotransposition in rodent cells.
  • Retrotransposition rates vary between human and rodent cells, suggesting host-specific modulation.

Conclusions:

  • The reduced retrotransposition efficiency of L1PA13A is attributable to both its ORF1p and ORF2p proteins.
  • Host cellular environment, potentially via ORF1p interactions, significantly impacts L1 retrotransposition efficiency.
  • Observed differences in activity between cell types may reflect evolutionary adaptations of L1 elements to their specific host genomes.