Cyclobutane pyrimidine dimers

Definition

Cyclobutane pyrimidine dimers (CPDs) are DNA lesions formed when adjacent pyrimidine bases, typically thymine or cytosine, become covalently bonded due to exposure to ultraviolet (UV) radiation. This dimerization disrupts normal base pairing and can lead to mutations if not repaired, highlighting the importance of DNA repair mechanisms in maintaining genomic integrity.

5 Must Know Facts For Your Next Test

1. CPDs are primarily caused by UV light exposure, particularly UV-B radiation, which is prevalent in sunlight.
2. The formation of CPDs can lead to replication errors during DNA synthesis if they are not repaired, resulting in permanent mutations.
3. Cells have evolved specific repair pathways, like nucleotide excision repair, to recognize and fix CPDs to prevent mutations from accumulating.
4. In organisms lacking effective DNA repair mechanisms, such as some forms of skin cancer, CPDs can accumulate and lead to tumorigenesis.
5. Measuring CPD levels can be an important biomarker for assessing UV exposure and the effectiveness of DNA repair processes in various organisms.

Review Questions

• What role do cyclobutane pyrimidine dimers play in the context of DNA mutations and repair mechanisms?
  • Cyclobutane pyrimidine dimers play a significant role in causing DNA mutations as they disrupt normal base pairing between nucleotides. When these dimers form due to UV radiation, they can lead to errors during DNA replication if not properly repaired. The cell employs various DNA repair mechanisms, particularly nucleotide excision repair, to recognize and rectify these dimers before they result in permanent genetic alterations.
• Discuss the impact of ultraviolet radiation on the formation of cyclobutane pyrimidine dimers and the subsequent cellular response.
  • Ultraviolet radiation, especially UV-B rays, directly induces the formation of cyclobutane pyrimidine dimers by causing adjacent pyrimidine bases to link together. This dimerization affects DNA structure and function, prompting the cell's response through specialized repair mechanisms such as nucleotide excision repair. If the cellular response is insufficient or defective, it can lead to increased mutation rates and potentially contribute to cancer development.
• Evaluate the consequences of inefficient repair of cyclobutane pyrimidine dimers in relation to long-term genetic stability and disease development.
  • Inefficient repair of cyclobutane pyrimidine dimers can significantly compromise long-term genetic stability by allowing mutations to accumulate within the genome. This accumulation increases the risk of oncogenic transformations and contributes to the development of diseases such as skin cancer. Understanding how cells manage CPDs through their repair mechanisms is crucial for developing strategies to mitigate UV-induced damage and prevent disease progression.

Related terms

DNA Repair: The collection of processes by which a cell identifies and corrects damage to its DNA molecules.

Ultraviolet Radiation: A form of electromagnetic radiation with wavelengths shorter than visible light, known to cause various types of DNA damage, including the formation of CPDs.

Nucleotide Excision Repair: A DNA repair mechanism that removes bulky DNA lesions, including cyclobutane pyrimidine dimers, and replaces them with the correct nucleotides.