Cells use two key methods to repair damaged DNA: nucleotide excision repair (NER) and base excision repair (BER). Both procedures are essential for protecting the genome’s integrity and avoiding mutations that might cause numerous illnesses, including cancer.
Cells use the DNA repair process known as nucleotide excision repair (NER) to fix a range of DNA lesions, including those brought on by UV radiation, chemical exposure, and other types of DNA damage. The integrity of the genetic data contained within the DNA molecule is the major goal of NER.
The two different NER sub-pathways known as global genome repair (GGR) and transcription-coupled repair (TCR) should be noted. While TCR primarily targets lesions that are preventing the progression of RNA polymerase during transcription, GGR targets lesions across the entire genome.
A highly conserved and crucial method for preserving the genomic stability of animals is nucleotide excision repair. Genetic conditions like Xeroderma Pigmentosum (XP), which is characterized by a high risk of developing skin cancer due to an inability to repair UV-induced DNA damage, can be brought on by flaws in the NER.
Base Excision Repair (BER) is a DNA repair process that is essential for preserving the integrity of our cells’ genetic material. Numerous sorts of damage, including chemical alterations to individual bases, can occur to DNA. BER focuses primarily on bases that have been damaged, such as bases that are aberrant or damaged due to factors including spontaneous chemical reactions, radiation exposure, or reactive oxygen species action.
By fixing little, localized damage to individual bases, Base Excision Repair is an essential procedure that aids in maintaining the integrity of DNA. These broken bases may cause mutations or flaws in the genetic code, which may result in different diseases, including cancer, if they are not fixed.
|
S.No. |
Aspect |
Nucleotide Excision Repair (NER) |
Base Excision Repair (BER) |
|
1 |
Repair Type |
Corrects bulky lesions and UV-induced damage |
Repairs small, non-bulky DNA lesions |
|
2 |
Lesion Size |
Repairs large DNA lesions |
Repairs small DNA lesions |
|
3 |
Damage Recognition |
Recognizes distortions in DNA structure |
Recognizes damaged or altered bases |
|
4 |
Enzyme Complexity |
Involves multiple enzymes and proteins |
Generally requires fewer enzymes |
|
5 |
Helicase Activity |
Requires helicase to unwind DNA strands |
Usually doesn’t require helicase |
|
6 |
Damaged Strand Removal |
Removes a single-strand segment |
Removes only the damaged base |
|
7 |
Strand Resynthesis |
Synthesizes a new strand using a template |
Uses the undamaged strand as a template |
|
8 |
Excised Nucleotides |
Removes multiple nucleotides |
Removes a single nucleotide |
|
9 |
Replication Machinery |
Involves polymerases δ or ε for synthesis |
Utilizes polymerase β for synthesis |
|
10 |
Prevalent DNA Damage Types |
Addresses a wide range of DNA lesions |
Primarily deals with oxidized bases |
|
11 |
Repair Speed |
Slower repair process |
Generally faster repair process |
|
12 |
Strand Breaks |
Creates temporary single-strand breaks |
Does not create strand breaks |
|
13 |
Role in Xeroderma Pigmentosum |
Deficiencies lead to Xeroderma Pigmentosum |
Not linked to Xeroderma Pigmentosum |
|
14 |
Excision Bubble Formation |
Forms an excision bubble during repair |
No excision bubble formation |
|
15 |
Repair Pathway |
Part of the global genome repair pathway |
Part of the single-strand repair pathway |
|
16 |
Recognition of Damaged Bases |
Less emphasis on damaged base recognition |
Emphasizes recognition of damaged bases |
|
17 |
Strand Break Signaling |
Induces DNA damage signaling |
Less likely to induce signaling |
|
18 |
Energy Requirements |
Requires more energy due to longer repair |
Requires less energy |
|
19 |
UV Light Sensitivity |
Efficient at repairing UV-induced damage |
Less efficient at UV damage repair |
|
20 |
Repair of Cyclobutane Pyrimidine Dimers |
Efficiently repairs these lesions |
Doesn’t directly repair them |
|
21 |
Repair of 8-oxoguanine |
Less efficient in repairing this lesion |
Efficiently repairs 8-oxoguanine |
|
22 |
Hereditary Disorders |
Mutations in NER genes lead to XP, CS, etc. |
BER deficiencies less commonly cause disorders |
|
23 |
Role in Tumor Suppression |
Plays a role in suppressing cancer |
Also contributes to cancer prevention |
|
24 |
Role in Aging |
Implicated in aging due to UV damage |
Influences aging through oxidation damage |
|
25 |
Role in Neurological Diseases |
Involved in certain neurological diseases |
Associated with some neurological disorders |
|
26 |
Importance in Mammals |
Highly conserved in mammals |
Present but less conserved in mammals |
|
27 |
Recognition of Distortions |
Recognizes helical distortions in DNA |
Emphasizes base-specific recognition |
|
28 |
Repair of Thymine Dimers |
Efficiently repairs thymine dimers |
Doesn’t repair thymine dimers |
|
29 |
Role in Transcription |
Can affect transcription due to strand breaks |
Less likely to affect transcription |
|
30 |
Prevalence in Eukaryotes |
Widespread in eukaryotes |
Found in all eukaryotes |
|
31 |
Role in Immune System |
Involved in somatic hypermutation |
Not directly linked to the immune system |
|
32 |
Repair of Alkylated Bases |
Less efficient at repairing alkylated bases |
Efficiently repairs alkylated bases |
|
33 |
Role in Repair Synthesis |
Often involves long-patch synthesis |
Usually involves short-patch synthesis |
|
34 |
Role in Cisplatin Resistance |
Can lead to cisplatin resistance when disrupted |
Not typically associated with cisplatin resistance |
|
35 |
Role in Ogg1 Protein |
Less emphasis on Ogg1 protein involvement |
Ogg1 plays a key role in BER |
|
36 |
Role in Strand Displacement |
Typically displaces longer DNA segments |
Usually displaces a single nucleotide |
|
37 |
Role in Chemotherapy |
NER deficiencies can impact chemotherapy success |
BER deficiencies less commonly impact chemotherapy |
|
38 |
Role in Oxidative Stress |
Less directly involved in oxidative stress response |
Part of the response to oxidative stress |
|
39 |
Repair of Bulky Adducts |
Efficiently repairs bulky DNA adducts |
Not specialized for bulky adduct repair |
|
40 |
Role in Ultraviolet Damage |
Primarily addresses UV-induced damage |
Less focused on UV damage repair |
|
41 |
Connection to Cockayne Syndrome |
Mutations can lead to Cockayne Syndrome |
Not directly connected to Cockayne Syndrome |
|
42 |
Role in Telomere Maintenance |
Not directly involved in telomere maintenance |
BER has some role in telomere maintenance |
|
43 |
Role in Chemotherapeutic Drugs |
Can affect response to certain chemotherapeutic drugs |
Less impact on chemotherapeutic drug responses |
|
44 |
Repair of Bulky DNA Lesions |
Specialized for repairing bulky DNA lesions |
Less effective at repairing bulky lesions |
|
45 |
Requirement for DNA Ligase |
Requires DNA ligase for strand sealing |
Requires DNA ligase for sealing gaps |
Frequently Asked Questions (FAQs)
Q1. What purpose does NER serve?
By mending lesions that could potentially cause mutations if left unattended, NER plays a key function in preserving the integrity of the genome.
Q2. What makes BER critical to cellular health?
The buildup of mutations brought on by various types of chemical damage to DNA bases must be stopped, and BER is essential for this. If these lesions are not repaired, there may be genetic instability and the emergence of illnesses like cancer.
Q3. Do NER and BER collaborate?
Yes, they can cooperate to fix many forms of DNA damage. Larger lesions are handled by NER, and if a lesion is not repaired or is handled improperly by NER, it may become a substrate for BER.
Q4. When should NER be used instead of BER, and vice versa?
For bigger lesions brought on by UV rays and toxins, NER is favored. For correcting more minor chemical alterations in specific bases, BER is appropriate.
Q5. What distinguishes NER from BER most significantly?
While BER concentrates on repairing individual damaged bases through a more focused process, NER fixes large lesions and requires the removal of a piece of DNA.
