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Chapter 15: Problem 14

Contrast the various types of DNA repair mechanisms known to counteract the effects of UV radiation. What is the role of visible light in repairing UV- induced mutations?

Short Answer

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Answer: The different DNA repair mechanisms that counteract the effects of UV radiation include photoreactivation (light repair), nucleotide excision repair (NER), and base excision repair (BER). Visible light plays a crucial role in repairing UV-induced mutations primarily through photoreactivation, where the enzyme photolyase absorbs energy from visible light to reverse the UV-induced damage. While photoreactivation is an efficient and specific repair mechanism, other repair mechanisms like NER and BER, which do not require light, also help deal with the diverse range of DNA damage caused by UV radiation.

Step by step solution

01

Introduction to DNA Repair Mechanisms for UV Radiation

UV radiation is harmful to living organisms as it can induce DNA damage, leading to mutations that may cause various diseases, including cancer. Organisms, however, have evolved different DNA repair mechanisms to counteract the effects of UV radiation. These mechanisms include photoreactivation, nucleotide excision repair, and base excision repair.
02

Photoreactivation (Light Repair)

Photoreactivation, also known as light repair or photoreversal, is a type of DNA repair mechanism that uses visible light to repair damage caused by UV radiation. A specialized enzyme called photolyase is responsible for this process. Photolyase absorbs energy from visible light (blue and near-UV wavelengths) to catalyze the reversal of UV-induced damage, primarily pyrimidine dimers. One important advantage of photoreactivation is that it is highly specific and does not introduce errors in the repaired DNA.
03

Nucleotide Excision Repair (NER)

Nucleotide excision repair (NER) is a versatile DNA repair mechanism that can remove a wide range of DNA lesions induced by UV radiation, such as pyrimidine dimers and bulky DNA adducts. The mechanism involves the identification and removal of a damaged section of the DNA strand, followed by resynthesis and ligation to restore the original sequence. Nucleotide excision repair is more complex than photoreactivation and involves the coordinated action of many proteins, including the XP proteins, Uvr proteins (in bacteria) and the Rad proteins (in yeast).
04

Base Excision Repair (BER)

Base excision repair (BER) is a simpler DNA repair mechanism that helps to repair individual damaged or incorrect bases caused by UV radiation or other sources. In this mechanism, a specific glycosylase enzyme recognizes the damaged or inappropriate base and cleaves it off the DNA strand, leaving an abasic site. This site is then processed and filled in by other enzymes, restoring the original DNA sequence. Base excision repair is less specific than photoreactivation or nucleotide excision repair, but it can deal with a broader range of DNA damage types.
05

Role of Visible Light in Repairing UV-induced Mutations

Visible light plays a crucial role in repairing UV-induced mutations, primarily through the mechanism of photoreactivation as mentioned earlier. The enzyme photolyase absorbs energy from visible light to reverse the UV-induced damage, facilitating the repair process. This enables certain organisms to use sunlight as a source of energy to repair DNA damage efficiently through photoreactivation. However, it is important to note that photoreactivation alone cannot repair all types of UV-induced lesions, and organisms rely on other repair mechanisms like NER and BER, which do not require light, to deal with the diverse range of DNA damage caused by UV radiation.

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Most popular questions from this chapter

In this chapter, we focused on how gene mutations arise and how cells repair DNA damage. At the same time, we found opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, (a) How do we know that mutations occur spontaneously? (b) How do we know that certain chemicals and wavelengths of radiation induce mutations in DNA? (c) How do we know that DNA repair mechanisms detect and correct the majority of spontaneous and induced mutations?

Suppose you are studying a DNA repair system, such as the nucleotide excision repair in vitro. By mistake, you add DNA ligase from a tube that has already expired. What would be the result?

Why would a mutation in a somatic cell of a multicellular organism escape detection?

Presented here are hypothetical findings from studies of heterokaryons formed from seven human xeroderma pigmentosum cell strains: $$\begin{array}{lccccccc} & X P 1 & X P 2 & X P 3 & X P 4 & X P 5 & X P 6 & X P 7 \\ X P 1 & \- & & & & & & \\ X P 2 & \- & \- & & & & & \\ X P 3 & \- & \- & \- & & & & \\ X P 4 & \+ & \+ & \+ & \- & & & \\ X P S & \+ & \+ & \+ & \+ & \- & & \\ X P 6 & \+ & \+ & \+ & \+ & \- & \- & \\ X P 7 & \+ & \+ & \+ & \+ & \- & \- & - \end{array}$$ These data are measurements of the occurrence or nonoccur- rence of unscheduled DNA synthesis in the fused heterokaryon. None of the strains alone shows any unscheduled DNA synthesis. Which strains fall into the same complementation groups? How many different groups are revealed based on these data? What can we conclude about the genetic basis of XP from these data?

The initial discovery of IS elements in bacteria revealed the presence of an element upstream \(\left(5^{\prime}\right)\) of three genes controlling galactose metabolism. All three genes were affected simultaneously, although there was only one IS insertion. Offer an explanation as to why this might occur.
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