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Chapter 5: Problem 96

How is the DNA damaged by ultraviolet light repaired?

Short Answer

Expert verified
DNA damage caused by ultraviolet (UV) light, such as the formation of pyrimidine dimers, is repaired through a process called nucleotide excision repair (NER). This process involves four main steps: (1) recognition of the damaged site by cellular proteins, (2) excision of the damaged DNA by enzymes like XPF-ERCC1 and XPG, (3) synthesis of a new DNA strand to fill the resulting gap by DNA polymerases using the intact complementary strand as a template, and (4) ligation of the newly synthesized DNA fragment to the original strand by DNA ligase. In some organisms, an alternative repair mechanism called photoreactivation can directly reverse UV-induced DNA damage using photolyase enzymes and visible light.

Step by step solution

01

Overview of DNA Damage by UV Light

Ultraviolet (UV) light, particularly UVB (280-315 nm wavelength) radiation, can cause DNA damage by inducing molecular changes in the DNA structure. These changes can interfere with the normal function of DNA and potentially lead to mutations and cell death. The most common form of DNA damage induced by UV light involves the formation of pyrimidine dimers, specifically cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6鈥�4) photoproducts (6鈥�4 PPs), between adjacent thymine or cytosine bases in DNA.
02

Recognition of DNA Damage

The first step in repairing UV-induced DNA damage is the recognition of the damaged site. Cellular proteins, such as those involved in the nucleotide excision repair (NER) pathway, scan the DNA and identify the distorted structure caused by the formation of pyrimidine dimers or other UV-induced DNA lesions.
03

Excision of the Damaged DNA

Once the damaged site is recognized, enzymes within the NER pathway, such as XPF-ERCC1 and XPG, cleave the DNA on both sides of the lesion to remove a small fragment containing the damaged bases. This process is called excision. In eukaryotes, this step is facilitated by proteins such as XPA, RPA, and the transcription factor IIH (TFIIH) complex.
04

DNA Synthesis and Gap Filling

After the damaged DNA fragment is removed, the resulting gap in the DNA strand needs to be filled. DNA polymerase enzymes synthesize a new stretch of DNA to replace the excised fragment, using the intact complementary DNA strand as a template. This process is called repair synthesis or gap filling.
05

DNA Ligation

The final step in repairing UV-induced DNA damage is the ligation of the newly synthesized DNA fragment to the original DNA strand. This process is carried out by DNA ligase, an enzyme that forms phosphodiester bonds to covalently join the two DNA fragments together, effectively sealing the gap and restoring the continuity of the DNA strand.
06

Alternative Repair Mechanism: Photoreactivation

In some organisms, an alternative DNA repair mechanism called photoreactivation can reverse UV-induced DNA damage. This process is mediated by photolyase enzymes, which use the energy from visible light to directly reverse the formation of pyrimidine dimers, thereby restoring the original DNA structure without the need for excision, synthesis, and ligation. However, this mechanism is not present in placental mammals, including humans.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Ultraviolet Light DNA Damage
Ultraviolet (UV) light is a part of the solar spectrum that can damage living organisms. One of the primary effects of UV light, especially UVB, is the damage it can cause to DNA. When DNA absorbs UV light, it undergoes changes. These can disrupt normal cellular processes. The most frequent problem is the formation of pyrimidine dimers. These occur between adjacent thymine or cytosine bases on the DNA strand.
  • Pyrimidine dimers lead to kinks in the DNA structure.
  • These structural changes prevent DNA from performing its regular functions.
  • This interference can result in mutations or cell death if not repaired.
The specific wavelengths that cause the most harm lie in the UVB range, between 280-315 nm.
Nucleotide Excision Repair
Nucleotide Excision Repair (NER) is a vital cellular mechanism. It plays a crucial role in fixing DNA damage, especially from UV light. This process identifies structural DNA distortions caused by damage and then repairs them. NER involves several steps:
  • Recognition: Specialized proteins identify the distorted sections of DNA.
  • Excision: Enzymes such as XPF-ERCC1 and XPG remove a short DNA segment containing the damaged bases.
  • Synthesis and Gap Filling: DNA polymerases synthesize a correct replacement for the excised fragment, using the undamaged strand as a guide.
  • Ligation: DNA ligase seals the newly synthesized DNA fragment back into the DNA strand, restoring its normal structure.
NER is present in all forms of life and is especially critical in humans and other eukaryotes.
Pyrimidine Dimers
Pyrimidine dimers are a direct result of UV light exposure. These molecules form when two adjacent pyrimidine bases, usually thymines, bond together excessively. When this happens, the DNA forms an unusual loop or kink, preventing it from being used properly by the cell. The two primary types of pyrimidine dimers are:
  • Cyclobutane Pyrimidine Dimers (CPDs): These are the most common. They form a four-membered ring structure.
  • Pyrimidine-Pyrimidone (6鈥�4) Photoproducts: These form less frequently but still significantly damage DNA.
Both types hinder DNA replication and transcription. Left unrepaired, they can have severe cellular consequences.
Photoreactivation
Photoreactivation is an alternative repair mechanism found in some organisms. This process is both fascinating and efficient in directly repairing UV-induced DNA damage without the need for cutting or synthesizing new DNA segments. Photoreactivation uses photolyase enzymes, which:
  • Absorb light energy, usually from the blue or visible spectrum.
  • Use this energy to break the bonds of pyrimidine dimers.
  • Restore the DNA to its original structure without additional synthesis or repair steps.
This process is especially advantageous as it is quick and does not require the intricate steps of NER. However, it's important to note that photoreactivation is absent in placental mammals, such as humans.

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Most popular questions from this chapter

A bacterial culture is divided into two halves, \(\mathrm{A}\) and \(\mathrm{B}\), and both halves receive large but equal amounts of ultraviolet light. Culture \(B\) is then wrapped in brown paper to isolate it from any light. Culture \(\mathrm{A}\) is left unprotected from the incident visible light. After 24 hours the cultures are examined. Culture A shows much more growth than culture \(B\). Explain.

Both Mr. and Mrs. Brown suffer from an autosomal recessive condition that makes them anemic. Mr. Brown has one amino acid substitution in the \(\beta\) -chain of his hemoglobin molecules and Mrs. Brown has a similar defect in her \(\alpha\) -chain. Neither Betsy nor Boopsy, their children, are anemic. Explain.

Photoreactivation and excision repair are two efficient repair mechanisms available to a cell which has undergone UV irradiation. However, extremely high doses of UV elicit a third type of repair system that greatly increases the rate of mutation. What is this system and why does it increase the mutation rate?

An actress with O type blood accused a producer with B type blood of being the father of her child in a paternity suit. The child was also O type. What does the blood type suggest about his guilt?

What are the different types of point mutations?
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