Pyrimidine dimers

Definition

Pyrimidine dimers are a type of DNA damage that occurs when two adjacent pyrimidine bases, usually thymine, bond together due to ultraviolet (UV) radiation. This abnormal covalent bond creates a distortion in the DNA structure, disrupting normal base pairing and leading to replication errors, which can result in mutations if not repaired effectively.

5 Must Know Facts For Your Next Test

1. Pyrimidine dimers are most commonly induced by UV light exposure, particularly UV-B radiation, leading to the covalent linking of adjacent thymine bases in the DNA strand.
2. If not repaired, pyrimidine dimers can cause serious mutations during DNA replication, as they hinder the normal base pairing process.
3. The presence of pyrimidine dimers can trigger cellular repair mechanisms, primarily nucleotide excision repair (NER), which is vital for maintaining genetic stability.
4. Certain organisms, such as bacteria and some fungi, possess specific photolyase enzymes that can directly reverse pyrimidine dimer formation using visible light.
5. In humans and other multicellular organisms, defects in repair mechanisms for pyrimidine dimers can lead to increased susceptibility to skin cancers and other UV-induced damage.

Review Questions

• How do pyrimidine dimers form, and what is their impact on DNA replication?
  • Pyrimidine dimers form when two adjacent pyrimidine bases, typically thymine, bond covalently due to UV radiation exposure. This bonding creates a distortion in the DNA structure, which disrupts normal base pairing. During DNA replication, this distortion can lead to errors as DNA polymerases struggle to accurately copy the damaged template strand, resulting in potential mutations.
• Discuss the role of nucleotide excision repair in addressing pyrimidine dimer damage.
  • Nucleotide excision repair (NER) plays a crucial role in fixing pyrimidine dimer damage by recognizing the distorted DNA structure created by these lesions. The NER pathway involves several steps: the damaged segment is excised by specific enzymes, and then DNA polymerase synthesizes new nucleotides to fill the gap. Finally, DNA ligase seals the newly synthesized strand, restoring the integrity of the DNA molecule and preventing potential mutations.
• Evaluate the consequences of impaired repair mechanisms for pyrimidine dimers in human health.
  • Impaired repair mechanisms for pyrimidine dimers significantly increase the risk of developing skin cancers and other UV-induced diseases in humans. For example, individuals with Xeroderma Pigmentosum exhibit a genetic defect in nucleotide excision repair pathways, leading to an inability to effectively repair UV-induced DNA damage. This heightened sensitivity to sunlight results in numerous skin lesions and a dramatically increased risk of skin cancer due to the accumulation of unrepaired mutations.

Related terms

UV Radiation: A form of electromagnetic radiation with wavelengths shorter than visible light, known to cause damage to DNA, including the formation of pyrimidine dimers.

Nucleotide Excision Repair (NER): A DNA repair mechanism that recognizes and removes damaged DNA segments, including those caused by pyrimidine dimers, and synthesizes new DNA to replace the excised segment.

Mutagenesis: The process by which changes in the DNA sequence occur, which can be triggered by various factors, including DNA damage from pyrimidine dimers.