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Related Concept Videos

Nucleotide Excision Repair01:08

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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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The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Related Experiment Video

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REXO5 promotes genomic integrity through regulating R-loop using its exonuclease activity.

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Leukemia
|July 30, 2024
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RNA Exonuclease 5 (REXO5) degrades RNA within R-loops, preventing DNA damage and supporting normal cell function. This discovery offers new insights into chronic myeloid leukemia (CML) pathogenesis.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Chronic myeloid leukemia (CML) pathogenesis involves altered gene expression, but underlying mechanisms remain unclear.
  • The BCR::ABL1 fusion gene drives CML progression by modulating gene expression.

Purpose of the Study:

  • To identify novel genes involved in CML pathogenesis.
  • To elucidate the molecular mechanisms of REXO5 in DNA damage response and CML.

Main Methods:

  • Utilized REXO5 knockout (KO) K562 cell lines and wild-type (WT) cells.
  • Investigated REXO5 translocation to DNA damage sites via its RNA recognition motif (RRM).
  • Assessed R-loop accumulation, DNA damage, and ATR-CHK1 activation in REXO5 KO cells.

Main Results:

  • REXO5 mRNA expression is elevated in CML patients.
  • REXO5 KO cells exhibit increased R-loops and DNA damage compared to WT cells.
  • REXO5 translocates to DNA damage sites, binds R-loops, and degrades mRNA via its exonuclease domain, regulating R-loop levels and ATR-CHK1 activation.

Conclusions:

  • REXO5 plays a critical role in the physiological control of R-loops through its exonuclease activity.
  • REXO5's function in R-loop regulation provides novel insights into CML pathogenesis.
  • Dysregulation of REXO5 may contribute to CML development and progression.