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PIWI-interacting RNAs, or piRNAs, are the most abundant short non-coding RNAs. More than 20,000 genes have been found in humans that code for piRNAs while only 2000 genes have been found for miRNAs. piRNAs can act at the transcriptional and post-transcriptional levels and have a vital role in silencing transposable elements present in germ cells. They are also involved in epigenetic silencing and activation. Previously, they were thought to function only in germ cells but new evidence suggests...
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LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
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Updated: Jun 1, 2025

RNA Next-Generation Sequencing and a Bioinformatics Pipeline to Identify Expressed LINE-1s at the Locus-Specific Level
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p53-mediated regulation of LINE1 retrotransposon-derived R-loops.

Pratyashaa Paul1, Arun Kumar1, Ankita Subhadarsani Parida1

  • 1Department of Biological Sciences, Indian Institute of Science Education and Research Berhampur, Berhampur, Odisha, India.

The Journal of Biological Chemistry
|January 19, 2025
PubMed
Summary

The tumor suppressor p53 prevents genomic instability by silencing Long Interspersed Nuclear Element 1 (LINE1) transposons. It inhibits the formation of RNA-DNA hybrids (R-loops) and works with histone methyltransferases to suppress L1 activation.

Keywords:
DNA damageL1/LINE1R-loopsRNA-DNA hybridsci R-loopgenomic instabilitylong noncoding RNAp53reverse transcriptiontrans R-loop

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Area of Science:

  • Genetics
  • Molecular Biology
  • Epigenetics

Background:

  • Long Interspersed Nuclear Element 1 (LINE1) retrotransposons are abundant in the human genome and can become active in cancer.
  • The tumor suppressor p53 has been shown to silence LINE1 elements, but the mechanisms are not fully understood.
  • RNA-DNA hybrids (R-loops) are intermediates in LINE1 retrotransposition.

Purpose of the Study:

  • To investigate the molecular mechanisms of p53-mediated repression of LINE1 elements and their intermediates.
  • To explore the role of p53 in regulating LINE1-derived R-loops.
  • To understand how p53 cooperates with epigenetic modifiers to control LINE1 activity.

Main Methods:

  • DNA-RNA immunoprecipitation-sequencing (DRIP-seq) to detect R-loops.
  • Experiments using p53-null (p53-/-) and wild-type (WT) cells.
  • Treatment with histone deacetylase inhibitors (HDACi) and reverse transcriptase inhibitors.
  • Analysis of histone modifications at LINE1 loci.

Main Results:

  • R-loop accumulation (cis and trans) was increased in p53-/- cells, synergizing with HDAC inhibitors.
  • Reverse transcriptase inhibition reduced R-loop levels, confirming the role of retrotransposition.
  • In WT cells, HDAC inhibitor withdrawal led to LINE1 suppression, marked by repressive histone marks (H3K9me3, H3K27me3) and reduced activating marks.
  • p53 collaborates with SETDB1 and G9A to deposit H3K9me3 at the LINE1 promoter, silencing transposons.

Conclusions:

  • p53 plays a novel role in preventing the formation of LINE1-derived R-loops.
  • p53 suppresses hyperactivated LINE1 elements by cooperating with histone methyltransferases.
  • These findings highlight p53's critical function in maintaining genomic stability through LINE1 regulation.