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Nucleotide Excision Repair01:38

Nucleotide Excision Repair

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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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The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular cells,...
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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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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Published on: August 21, 2021

DNA repair during embryonic epidermal stratification.

Fumiya Meguro1,2,3, Katsushige Kawasaki1,4, Yoshito Kakihara2

  • 1Division of Oral Anatomy, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|May 29, 2025
PubMed
Summary
This summary is machine-generated.

DNA repair mechanisms involving Reptin are crucial for embryonic skin development. Deleting Reptin in mice prevents epidermal stratification due to DNA damage, highlighting its role in organogenesis.

Keywords:
DNA damageReptinepidermisp53skin development

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Genomes face constant DNA damage from various agents.
  • DNA repair mechanisms are vital for genome integrity.
  • The necessity of DNA repair for organogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of DNA repair mechanisms in embryonic organogenesis, specifically skin development.
  • To determine if the DNA repair molecule Reptin is essential for epidermal stratification.

Main Methods:

  • Utilized conditional gene deletion in mice to specifically remove the Reptin gene in epidermal cells (Reptinfl/fl;K14Cre).
  • Analyzed epidermal structure, DNA damage levels, cell proliferation, and p53 expression in mutant and wild-type mice.
  • Generated double mutant mice (Reptinfl/fl;K14Cre;p53-/-) to assess the role of p53 in Reptin-deficient epidermis.

Main Results:

  • Epithelial-specific deletion of Reptin in mice (Reptinfl/fl;K14Cre) resulted in a failure of epidermal stratification.
  • Mutant epidermis exhibited significant DNA damage, reduced cell proliferation, and increased p53 expression compared to wild-type.
  • Simultaneous deletion of p53 restored epidermal stratification in Reptin-deficient mice, indicating p53's involvement in the phenotype.

Conclusions:

  • DNA damage likely occurs during embryonic epidermal stratification.
  • The DNA repair molecule Reptin plays a critical role in repairing this damage and enabling stratification.
  • Reptin-mediated DNA repair is essential for proper skin organogenesis.