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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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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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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Analysis of LINE-1 Retrotransposition at the Single Nucleus Level
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The Nucleotide Excision Repair Pathway Limits L1 Retrotransposition.

Geraldine Servant1,2, Vincent A Streva1,2, Rebecca S Derbes1,2

  • 1Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane Cancer Center, Tulane University, New Orleans, Louisiana 70112.

Genetics
|January 5, 2017
PubMed
Summary
This summary is machine-generated.

The nucleotide excision repair (NER) pathway limits L1 retrotransposition, preventing insertional mutations and large genomic duplications. NER proteins like XPD, XPA, and XPC are crucial for maintaining genome integrity against mobile elements.

Keywords:
DNA damageL1 retrotransposongenome stabilitynucleotide excision repairtarget-primed reverse transcription

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Area of Science:

  • Genetics
  • Molecular Biology
  • Genomics

Background:

  • Long interspersed elements 1 (L1) are mobile genetic elements comprising 17% of the human genome.
  • L1 retrotransposition can cause genetic diseases through de novo insertions.
  • The ERCC1-XPF endonuclease complex is known to limit L1 retrotransposition.

Purpose of the Study:

  • To investigate the role of the nucleotide excision repair (NER) pathway in preventing L1 retrotransposition.
  • To determine if NER proteins are involved in limiting the insertion of retroelements into the genome.
  • To explore the potential role of NER in preventing genomic instability at retrotransposon insertion sites.

Main Methods:

  • Monitoring retrotransposition efficiencies of engineered L1 elements in NER-deficient and complemented cell lines.
  • Analyzing de novo L1 inserts and their genomic locations in NER-deficient cells.
  • Assessing the involvement of core NER proteins (XPD, XPA) and XPC in L1 retrotransposition.

Main Results:

  • NER-deficient cells exhibited increased L1 retrotransposition efficiencies.
  • Core NER proteins (XPD, XPA) and XPC were found to limit L1 retrotransposition.
  • Abnormally large duplications were observed at L1 insertion sites in NER-deficient cells.

Conclusions:

  • The NER pathway plays a significant role in limiting L1 retrotransposition and preventing insertional mutations.
  • NER proteins are involved in preventing potentially mutagenic large genomic duplications at retrotransposon insertion sites.
  • NER pathway contributes to genome integrity by suppressing retrotransposon-mediated mutations and duplications.