Light repair (photoreactivation)
Light repair is a mechanism for restoring the structure of DNA damaged by ultraviolet (UV) radiation. Under the influence of UV light, pathological cross-links—pyrimidine dimers—are formed in the genetic code. These include thymine, cytosine, and mixed thymine-cytosine dimers.
To eliminate these defects, the cell uses a specialized enzyme—photolyase. The repair process is triggered exclusively upon the absorption of a quantum of visible light. The mechanism consists of the following steps:
- Photolyase recognizes the damage and binds to the region of the formed dimer.
- Activated by light, the enzyme cleaves the incorrect bonds between adjacent pyrimidine bases.
- The spatial structure of the DNA molecule returns to normal.
Excision repair
The name of the process comes from the Latin word excision, which translates as "cutting out." This is a complex multi-step mechanism whose essence lies in the physical removal of the damaged segment of the strand. There are two main types based on timing: pre-replicative repair (occurring in the $G_1$-period of the cell cycle, before DNA duplication begins) and replicative repair (occurring directly during replication).
The mechanism of excision repair is strictly sequential:
- Recognition and incision (cutting). Specific enzymes, primarily endonuclease, scan the DNA, recognize the damaged fragment, and carefully excise it.
- Resynthesis. The enzyme DNA polymerase goes to work. Using the undamaged complementary strand as a template, it synthesizes new nucleotides and fills the resulting gap.
- Ligation (joining). The enzyme ligase joins (stitches) the ends of the newly synthesized fragment to the main strand of the molecule, fully restoring its integrity.
Separately, replicative repair is considered, which corrects nucleotide mismatch errors right during synthesis. If non-complementary bases are incorporated into the daughter strand (violating Chargaff's rule: A=T, G=C), incorrect pairs are formed. In biology, such non-complementary pairs are called mismatches (from English mismatch).
Post-replication and SOS repair
If damage was not eliminated before or during the duplication of genetic material, the cell engages backup systems.
Post-replication repair is carried out in the $G_2$-period of the cell cycle (after replication has already occurred). Its mechanism is based on the process of recombination—the exchange of fragments between two new DNA helices. If a defect remains in the template strand (e.g., a thymine dimer), DNA polymerase cannot pass through it, and a "gap" is formed in the newly synthesized strand. This gap is filled by a segment from the corresponding strand of the second daughter molecule. Then, the integrity of the first daughter strand is restored, and the missing fragment in the second molecule is synthesized based on the complementary template.
SOS repair is an emergency rescue mechanism discovered by Miroslav Radman in 1974. It is triggered when the cell needs to complete replication, but multiple unresolved defects are present in the DNA. The main goal is to modify the damaged region so as to lift the replication block. To achieve this, the cell induces the synthesis of a special protein that binds to DNA polymerase. The modified enzyme acquires the ability to extend the daughter strand even opposite defective template links. As a result, the DNA is successfully duplicated and the cell continues to divide, but pays for this with a huge number of mutations (errors).
Clinical significance: repair system pathologies
Failures in repair mechanisms are directly linked to the development of hereditary diseases and oncogenesis. It is believed that up to 90% of all oncological diseases may be caused by impairments in DNA repair systems.
A striking example of a pathology arising from a defect in repair systems is xeroderma pigmentosum (Xeroderma pigmentosum). The etiological nature of this disease was proven by researcher James Cleaver in 1968. One of the forms of xeroderma is based on a significant decrease or complete loss of activity of the enzyme UV-endonuclease.
The clinical picture begins with the appearance of characteristic red spots on the skin upon exposure to ultraviolet light. Over time, these lesions develop into progressive crusts and ultimately transform into a malignant tumor. This disease is incurable, as the cell completely loses the ability to repair UV damage.
Briefly: answers to topical questions
What is the difference between base excision repair (BER) and nucleotide excision repair (NER)?
The difference between base excision repair (BER) and nucleotide excision repair (NER) lies in the type of damage repaired and the set of specific enzymes involved.
| Characteristic | BER | NER |
|---|---|---|
| Type of damage | Do not heavily distort the helix structure (e.g., deamination) | Bulky damage distorting the helix (pyrimidine dimers) |
| Recognizing enzyme | DNA glycosylase | Specific protein complex |
| Strand incision | AP endonuclease cuts the backbone at the AP site | UV endonuclease makes incisions at the 3' and 5' ends |
| DNA synthesis | DNA polymerase $\beta$ | DNA polymerase $\delta$ or $\epsilon$ |
To memorize the three main stages of excision repair, use the abbreviation "URI": Understanding/Recognition (endonuclease cuts), Resynthesis (DNA polymerase builds), Ligation (ligase joins).
Class and exam questions
Which enzyme is key in the process of photoreactivation?
The main role is played by the enzyme photolyase. Upon activation by a quantum of visible light, it cleaves the bonds in pyrimidine dimers formed under the influence of UV radiation.
What is a "mismatch"?
A mismatch (English mismatch) is a nucleotide pairing error in which non-complementary bases are incorporated into the daughter DNA strand, violating Chargaff's rule.
What is the danger of SOS repair for the cell?
The SOS system allows DNA polymerase to ignore template damage in order to complete DNA duplication at any cost. As a result, the cell survives and divides, but accumulates a huge number of potentially dangerous mutations.
What else to study on this topic
- Structure and functions of the photolyase enzyme
- Mechanism of thymine dimer formation under UV irradiation
- The process of genetic recombination in post-replication repair
- Molecular bases of the pathogenesis of xeroderma pigmentosum
Master the entire topic in the "Biology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "DNA Repair" and 3,793 other pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 129 video lessons on the subject
Other topics in "Molecular Genetics"
Free video lessons: BiologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.