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Related Concept Videos

Non-LTR Retrotransposons03:18

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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
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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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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Related Experiment Video

Updated: Dec 5, 2025

RNA Next-Generation Sequencing and a Bioinformatics Pipeline to Identify Expressed LINE-1s at the Locus-Specific Level
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p53 directly represses human LINE1 transposons.

Bhavana Tiwari1, Amanda E Jones1, Candace J Caillet1

  • 1Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

Genes & Development
|October 16, 2020
PubMed
Summary

The tumor suppressor p53 restricts mobile DNA elements called LINE1s in human cells. Loss of p53 causes LINE1s to become active, leading to genomic instability and cancer threats.

Keywords:
LINE1p53transrepressiontumor suppressors

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Analysis of LINE-1 Retrotransposition at the Single Nucleus Level
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Analysis of LINE-1 Retrotransposition at the Single Nucleus Level

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The p53 protein is a critical tumor suppressor frequently altered in human cancers.
  • Previous studies showed p53 restricts retrotransposons in germline cells of model organisms.
  • The role of p53 in controlling retrotransposons in human somatic cells remained unclear.

Purpose of the Study:

  • To investigate whether p53 restricts LINE1 retrotransposons in human somatic cells.
  • To understand the mechanism by which p53 regulates LINE1 activity.
  • To determine the consequences of p53 loss on LINE1 activity and genomic stability.

Main Methods:

  • ChIP-sequencing to identify p53 binding sites on LINE1 elements.
  • Analysis of histone modifications at LINE1 loci.
  • Assessing LINE1 activity and chromosomal rearrangements upon p53 depletion or disruption of p53 binding sites.
  • Investigating inflammatory responses dependent on LINE1 reverse transcriptase.

Main Results:

  • p53 directly binds to the 5'UTR of human LINE1 elements.
  • p53 promotes repressive histone marks at LINE1 promoters, restricting their activity.
  • Loss of p53 leads to LINE1 hyperactivity, chromosomal rearrangements, and inflammation.
  • LINE1 reverse transcriptase activity is crucial for the oncogenic threats observed in p53-deficient cells.

Conclusions:

  • p53 constitutively suppresses LINE1 retrotransposons in human somatic cells.
  • p53's regulation of LINE1s contributes to its tumor suppressor function by preventing genomic instability and oncogenic inflammation.
  • LINE1 elements pose acute oncogenic threats when p53's suppressive activity is lost.