14.6 DNA Repair
3 min read•june 14, 2024
DNA are changes in genetic material that can have profound effects on organisms. These alterations range from single nucleotide changes to large-scale chromosomal rearrangements, potentially impacting protein function and gene expression. Understanding mutations is crucial for grasping genetic disorders and evolution.
Fortunately, cells have evolved sophisticated repair mechanisms to maintain DNA integrity. These processes, including , , and , work tirelessly to fix damage and prevent mutations. When repair systems fail, it can lead to various diseases, highlighting the importance of DNA maintenance in health.
DNA Mutations and Repair Mechanisms
Types and effects of DNA mutations
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- : changes codon but still codes for same amino acid (GGG to GGA, both code for glycine)
- : changes codon resulting in different amino acid (GAG to GTG, changes glutamic acid to valine)
- : changes codon resulting in premature stop codon (CAG to TAG, changes glutamine to stop)
- : adds one or more nucleotides (ATGCATGC to ATGCATGCA)
- : removes one or more nucleotides (ATGCATGC to ATGATGC)
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- Insertion or deletion of nucleotides not divisible by three (ATGCATGCA to ATGCATCA)
- Alters reading frame affecting all downstream codons (changes amino acid sequence)
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- Large-scale changes in chromosome structure or number
- Deletions (loss of chromosome segment), duplications (extra copies of segment), inversions (reversed orientation of segment), translocations (exchange of segments between non-homologous chromosomes)
- Potential effects of mutations
- Alters protein function or structure (sickle cell anemia, abnormal hemoglobin)
- Causes loss of protein function (cystic fibrosis, non-functional CFTR protein)
- Leads to gain of abnormal function (oncogenes, uncontrolled cell growth)
- Changes gene expression (thalassemia, reduced globin production)
- Results in genetic disorders and diseases (Huntington's disease, progressive neurodegeneration)
Mechanisms of cellular DNA repair
- Direct reversal
- : uses light to repair UV-induced thymine dimers ()
- : removes alkyl groups from guanine residues ()
- Base excision repair (BER)
- recognize and remove damaged bases (, )
- cleaves DNA backbone at abasic site ()
- DNA polymerase fills gap and ligase seals nick (short-patch BER)
- (NER)
- Recognizes bulky DNA lesions such as UV-induced pyrimidine dimers ()
- Excises oligonucleotide containing damaged bases (27-29 nucleotides in humans)
- DNA polymerase fills gap and ligase seals nick (transcription-coupled NER, global genome NER)
- Mismatch repair (MMR)
- Recognizes mismatched bases during replication (G-T, A-C mismatches)
- Excises newly synthesized strand containing mismatch (strand discrimination by nicks)
- Resynthesizes excised strand by DNA polymerase (, complexes)
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- (HR): uses sister chromatid as template (error-free)
- (NHEJ): directly ligates broken ends (error-prone)
Key enzymes in DNA repair
- : synthesize new DNA strands to replace damaged or excised segments
- : seal nicks in the DNA backbone after repair synthesis
- : relieve torsional stress and untangle DNA during repair processes
- : unwind DNA to allow access for repair enzymes
- : exonuclease activity of some DNA polymerases corrects errors during replication
DNA repair defects and disease
- (XP)
- Defects in genes (, , , , , , )
- Increases sensitivity to UV light (1000-fold higher risk of skin cancer)
- Leads to high risk of skin cancer (basal cell carcinoma, squamous cell carcinoma, melanoma)
- Hereditary nonpolyposis colorectal cancer (HNPCC or )
- Defects in mismatch repair genes such as , (autosomal dominant)
- Increases risk of colorectal, endometrial and other cancers (lifetime risk up to 80%)
- (AT)
- Defects in gene involved in double-strand break repair (cell cycle checkpoint kinase)
- Causes progressive neurodegeneration, immunodeficiency and cancer predisposition (leukemia, lymphoma)
- (FA)
- Defects in genes involved in repair of DNA interstrand crosslinks (, , , etc.)
- Results in bone marrow failure, congenital abnormalities and cancer predisposition (acute myeloid leukemia)
- (BS)
- Defects in gene involved in homologous recombination (RecQ helicase)
- Leads to growth retardation, immunodeficiency and cancer predisposition (leukemia, lymphoma, solid tumors)
Key Terms to Review (58)
8-oxoguanine: 8-oxoguanine is a modified form of the nucleotide guanine that occurs when DNA is exposed to oxidative stress, often resulting from reactive oxygen species. This alteration can lead to mispairing during DNA replication, causing mutations and potentially contributing to various diseases, including cancer. The presence of 8-oxoguanine highlights the importance of DNA repair mechanisms that can recognize and correct such modifications to maintain genomic integrity.
AP endonuclease: AP endonuclease is an enzyme that plays a crucial role in the base excision repair pathway by recognizing and cleaving apurinic/apyrimidinic (AP) sites in DNA. These AP sites occur when a nitrogenous base is lost, leaving a gap in the DNA strand that can lead to mutations if not repaired. This enzyme facilitates the removal of damaged DNA, allowing for proper repair mechanisms to restore the integrity of the genetic material.
Apurinic/apyrimidinic site: An apurinic/apyrimidinic (AP) site is a location in DNA that has lost a purine or pyrimidine base, resulting in a gap that can interfere with proper DNA function. These sites are critical intermediates formed during the process of DNA damage and repair, highlighting the dynamic nature of the genome and the importance of maintaining genetic integrity. The presence of AP sites can lead to mutations if not properly repaired, connecting them directly to various DNA repair mechanisms and cellular responses to damage.
Ataxia telangiectasia: Ataxia telangiectasia is a rare genetic disorder that affects the nervous and immune systems, leading to symptoms such as progressive ataxia, telangiectasia (small dilated blood vessels), and increased susceptibility to infections and cancer. This disorder is primarily linked to mutations in the ATM gene, which plays a crucial role in DNA repair mechanisms, particularly in response to DNA double-strand breaks.
ATM: ATM (Ataxia Telangiectasia Mutated) is a crucial protein kinase that plays a vital role in the cellular response to DNA damage, particularly in the detection and repair processes. This protein is essential for maintaining genomic stability, as it initiates signaling cascades that lead to cell cycle arrest, DNA repair, and apoptosis in response to double-strand breaks in DNA. ATM is part of a larger network of proteins that communicate and coordinate cellular responses to various forms of stress, including radiation and other genotoxic agents.
Base excision repair: Base excision repair is a cellular mechanism that corrects DNA damage, specifically small, non-helix-distorting base lesions. This process plays a crucial role in maintaining genome integrity by removing and replacing damaged bases, which can arise from factors like oxidative stress or deamination. By recognizing and fixing these lesions, base excision repair helps prevent mutations that could lead to diseases like cancer.
BLM: BLM stands for Base Excision Repair, a crucial DNA repair mechanism that removes damaged or non-canonical bases from the DNA strand and replaces them with the correct ones. This process is vital for maintaining genomic stability, as it helps prevent mutations that could lead to various diseases, including cancer. BLM also refers to the Bloom syndrome gene, which plays a significant role in the maintenance of DNA integrity and repair processes, linking it directly to cellular responses to DNA damage.
Bloom syndrome: Bloom syndrome is a rare genetic disorder characterized by growth deficiencies, sun-sensitive skin, and an increased risk of cancer. It is caused by mutations in the BLM gene, which is essential for proper DNA repair and maintenance of genomic stability, linking it to the process of DNA repair.
Chromosomal mutations: Chromosomal mutations refer to alterations in the structure or number of chromosomes, which can lead to significant changes in an organism's genetic makeup. These mutations can result from various processes, such as errors during DNA replication, exposure to radiation, or chemical agents. The impact of chromosomal mutations extends to essential biological processes, influencing gene expression and contributing to genetic diversity within populations.
Cyclobutane pyrimidine dimers: Cyclobutane pyrimidine dimers (CPDs) are a type of DNA lesion formed when two adjacent pyrimidine bases, typically thymine, become covalently bonded due to exposure to ultraviolet (UV) light. These dimers distort the DNA structure, leading to replication errors and potential mutations if not repaired, making them critical in the study of DNA repair mechanisms.
Deletion: Deletion refers to a type of mutation where a segment of DNA is lost or removed from a chromosome. This can result in significant changes to gene function and expression, leading to inherited disorders or diseases. Deletions can occur in various sizes, from a single nucleotide to larger sections of the chromosome, impacting the organism's phenotype and potentially disrupting normal biological processes.
Direct reversal: Direct reversal is a DNA repair mechanism that restores the original DNA sequence without the need for template DNA. This process primarily corrects specific types of damage, such as those caused by alkylating agents or UV light, effectively reversing the modifications made to the DNA bases. This method is crucial for maintaining genetic stability and preventing mutations, showcasing the efficiency of cellular repair systems.
DNA ligases: DNA ligases are essential enzymes that catalyze the joining of DNA strands together by forming phosphodiester bonds, thus sealing nicks or breaks in the DNA backbone. These enzymes play a crucial role in various cellular processes, including DNA replication, repair, and recombination, ensuring the integrity and stability of the genetic material.
DNA polymerases: DNA polymerases are essential enzymes that synthesize new strands of DNA by adding nucleotides to a pre-existing strand during DNA replication. They play a crucial role in copying the genetic material, ensuring that the daughter cells receive an accurate copy of the DNA. Additionally, they are involved in DNA repair processes, correcting any mistakes that may occur during DNA replication or as a result of damage.
Double-strand break repair: Double-strand break repair refers to the cellular mechanisms that fix breaks in both strands of the DNA helix, which can be caused by various factors such as radiation, chemical exposure, or replication errors. This process is crucial for maintaining genomic stability and preventing mutations that could lead to diseases like cancer. There are two main pathways for repairing double-strand breaks: homologous recombination and non-homologous end joining, both of which play vital roles in cellular health and function.
FANCA: FANCA is a gene that encodes a protein involved in the Fanconi anemia (FA) DNA repair pathway, which is crucial for maintaining genomic stability. This gene plays a significant role in repairing interstrand cross-links, which can impede DNA replication and lead to cellular damage if left unaddressed. Mutations in FANCA can lead to Fanconi anemia, a genetic disorder characterized by increased sensitivity to DNA cross-linking agents, bone marrow failure, and a predisposition to cancers.
FANCB: FANCB refers to the Fanconi Anemia Complementation Group B, which is a protein complex involved in DNA repair mechanisms, particularly in the repair of interstrand cross-links. This complex plays a crucial role in maintaining genomic stability by recognizing DNA damage and facilitating its repair through homologous recombination. Defects in FANCB can lead to Fanconi anemia, a genetic disorder characterized by increased sensitivity to DNA-damaging agents and a predisposition to cancer.
FANCC: FANCC is a gene that encodes a protein involved in the DNA repair process, specifically in the Fanconi anemia pathway. This gene plays a crucial role in maintaining genomic stability by repairing DNA interstrand crosslinks, which can be harmful and lead to cellular dysfunction. Mutations in FANCC are linked to Fanconi anemia, a genetic disorder characterized by increased susceptibility to cancer and bone marrow failure.
Fanconi anemia: Fanconi anemia is a rare genetic disorder characterized by increased susceptibility to cancer, particularly leukemia, and various physical abnormalities. It primarily results from mutations in genes responsible for DNA repair mechanisms, specifically those involved in the repair of interstrand cross-links in DNA. This condition highlights the critical role of DNA repair pathways in maintaining genomic stability and preventing malignancies.
Frameshift mutations: Frameshift mutations are genetic alterations that occur when nucleotides are added to or deleted from the DNA sequence in a number that is not a multiple of three. This results in a shift in the reading frame of the gene, leading to changes in the amino acid sequence of the resulting protein. Such mutations can have severe effects on protein function and contribute to various genetic disorders.
Glycosylases: Glycosylases are a type of DNA repair enzyme responsible for recognizing and removing damaged or mismatched bases from DNA. They play a crucial role in the base excision repair pathway, which is essential for maintaining genomic integrity by fixing various types of DNA lesions, including those caused by oxidative stress and chemical damage. By facilitating the removal of incorrect bases, glycosylases help to prevent mutations that could lead to diseases, including cancer.
Helicases: Helicases are specialized enzymes that unwind and separate the two strands of DNA during processes such as replication and repair. This unwinding is crucial because it creates the single-stranded DNA templates needed for synthesis of new strands or for the repair mechanisms to function effectively.
Homologous recombination: Homologous recombination is a biological process where two similar or identical strands of DNA exchange genetic information, resulting in a mixture of parental alleles in the offspring. This process plays a critical role in repairing damaged DNA and ensuring the accurate segregation of chromosomes during cell division, particularly meiosis. By utilizing a homologous template, it facilitates genetic diversity and the maintenance of genomic stability.
Induced mutations: Induced mutations are changes in the DNA sequence caused by external agents such as chemicals or radiation. These mutations can alter gene function and potentially lead to various biological consequences, including diseases.
Insertion: Insertion refers to a type of mutation where one or more nucleotide bases are added into a DNA sequence, resulting in a change in the genetic code. This alteration can disrupt the normal function of genes, potentially leading to various biological effects such as disease or altered protein function. Insertions can occur due to errors during DNA replication or repair processes, and understanding them is essential in the context of how cells maintain genomic integrity.
Lynch syndrome: Lynch syndrome is a genetic disorder that significantly increases the risk of developing various types of cancer, particularly colorectal cancer and endometrial cancer. It is caused by mutations in genes responsible for DNA mismatch repair, leading to an accumulation of genetic errors that can result in tumor formation. Understanding Lynch syndrome is crucial as it has implications for both individual patients and their families regarding cancer screening and prevention strategies.
Methyltransferases: Methyltransferases are enzymes that transfer a methyl group ($$-CH_3$$) from a donor molecule, often S-adenosylmethionine (SAM), to specific substrates, including DNA, RNA, and proteins. These enzymes play crucial roles in various biological processes, such as gene expression regulation and DNA repair mechanisms, influencing how genetic information is maintained and expressed.
Mismatch repair: Mismatch repair is a crucial cellular mechanism that identifies and corrects errors that occur during DNA replication, specifically mismatches between the base pairs. This process ensures the fidelity of DNA by recognizing improperly paired nucleotides and replacing them with the correct ones, preventing potential mutations that could lead to diseases. Mismatch repair is vital for maintaining genomic stability and plays a significant role in DNA repair pathways, working alongside other systems to preserve genetic information.
Missense mutation: A missense mutation is a type of genetic alteration where a single nucleotide change results in the substitution of one amino acid for another in a protein. This alteration can affect the protein's function, potentially leading to various diseases or conditions. Missense mutations occur during DNA replication and can be corrected by specific DNA repair mechanisms, highlighting their significance in the context of maintaining genetic stability.
MLH1: MLH1 is a gene that encodes a protein involved in DNA mismatch repair, a crucial process for maintaining genetic stability by correcting errors that occur during DNA replication. This gene is part of the MMR pathway, which helps prevent mutations from being passed on to daughter cells, thus playing a significant role in cancer prevention, particularly in hereditary nonpolyposis colorectal cancer (Lynch syndrome). MLH1 functions as a vital player in identifying and repairing mismatched base pairs, ensuring the integrity of the genetic material.
MSH2: MSH2 is a key protein involved in the DNA mismatch repair system, which is responsible for correcting errors that occur during DNA replication. This protein plays a critical role in maintaining genomic stability by detecting and repairing mispaired nucleotides, thereby preventing mutations that can lead to cancer and other genetic disorders. Mutations in MSH2 can result in a higher risk of developing Lynch syndrome, a hereditary condition associated with several types of cancer.
Mutations: Mutations are changes in the nucleotide sequence of DNA, which can occur spontaneously or due to environmental factors. They can result in alterations to gene function and affect an organism's phenotype.
MutLα: MutLα is a protein complex that plays a critical role in the DNA mismatch repair (MMR) system, which is responsible for correcting errors that occur during DNA replication. This complex consists of two main proteins, MLH1 and PMS2, and it acts as a key player in identifying and repairing mispaired bases in the DNA helix, helping to maintain genomic stability and prevent mutations.
MutSα: MutSα is a protein complex that plays a crucial role in the DNA mismatch repair (MMR) system, which is essential for maintaining genomic stability by correcting errors that occur during DNA replication. Composed of two subunits, MSH2 and MSH6, MutSα recognizes and binds to mismatches in the DNA helix, initiating the repair process to prevent mutations that could lead to diseases such as cancer.
Non-homologous end joining: Non-homologous end joining (NHEJ) is a crucial DNA repair mechanism that directly joins broken ends of double-stranded DNA without the need for a homologous template. This process is essential for maintaining genome stability, particularly in response to DNA damage caused by various environmental factors or cellular processes. NHEJ is often utilized in cells that are in the G1 phase of the cell cycle when homologous recombination is not available.
Nonsense mutation: A nonsense mutation is a type of genetic alteration that changes a codon in DNA to a stop codon, resulting in premature termination of protein synthesis. This can lead to incomplete proteins that are often nonfunctional, which can significantly impact cellular function and contribute to various genetic disorders. Understanding how nonsense mutations affect protein translation is crucial in the context of DNA repair mechanisms, as cells possess pathways to correct such mutations to maintain genetic integrity.
Nucleotide excision repair: Nucleotide excision repair (NER) is a DNA repair mechanism that removes bulky, helix-distorting lesions such as thymine dimers. It involves the recognition of damage, excision of a short single-stranded DNA segment containing the lesion, and synthesis of a new strand using the undamaged strand as a template.
Nucleotide excision repair: Nucleotide excision repair is a cellular mechanism that identifies and removes damaged DNA segments, particularly those caused by UV light or chemical exposure, and replaces them with the correct nucleotides. This repair process is crucial for maintaining genomic stability and preventing mutations that could lead to various diseases, including cancer. It involves several key steps including damage recognition, excision of the damaged strand, DNA synthesis, and ligation.
O6-methylguanine: O6-methylguanine is a DNA lesion that occurs when a methyl group is added to the oxygen atom at the 6th position of guanine. This modification can lead to mispairing during DNA replication, potentially causing mutations if not repaired. It is a critical focus in understanding how cells maintain genetic stability and integrity through various DNA repair mechanisms.
Photoreactivation: Photoreactivation is a DNA repair mechanism that directly reverses the damage caused by ultraviolet (UV) light, specifically the formation of pyrimidine dimers in DNA. This process involves the activation of photolyase enzymes, which use light energy to cleave the bonds between the dimerized thymine bases, restoring the DNA to its original state. Photoreactivation is an important mechanism for maintaining genetic stability and preventing mutations caused by UV exposure.
Point mutations: Point mutations are changes in a single nucleotide base pair in DNA, which can lead to alterations in gene expression or function. These mutations can occur due to various factors, such as errors during DNA replication or exposure to environmental mutagens. The significance of point mutations extends into critical areas like DNA repair mechanisms and the study of genetic variation within populations, highlighting their role in evolution and adaptation.
Proofreading: Proofreading is a crucial process that occurs during DNA replication where the DNA polymerase enzyme checks and corrects errors in newly synthesized DNA strands. This process ensures high fidelity in DNA replication by allowing the enzyme to detect mismatched base pairs and replace them with the correct nucleotides, significantly reducing the chances of mutations. Proofreading enhances genetic stability and is vital for maintaining the integrity of the organism's genetic information.
Pyrimidine dimers: Pyrimidine dimers are covalent linkages formed between two adjacent pyrimidine bases, usually thymine, in DNA. This type of damage is primarily caused by ultraviolet (UV) radiation and can lead to distortions in the DNA structure, ultimately interfering with replication and transcription processes if left unrepaired. The formation of these dimers is a significant mutagenic event that poses a risk for various cellular functions and can contribute to skin cancer and other diseases.
Silent mutation: A silent mutation is a change in the DNA sequence that does not alter the amino acid sequence of the resulting protein. These mutations typically occur in the coding region of a gene but do not affect the protein's functionality. Silent mutations highlight the redundancy in the genetic code, where multiple codons can encode the same amino acid without any change in the protein's structure or function.
Spontaneous mutations: Spontaneous mutations are changes in DNA sequence that occur naturally without any external influence. These mutations arise during normal cellular processes such as DNA replication and repair.
Substitution: Substitution refers to a specific type of mutation in which one nucleotide base is replaced by another in the DNA sequence. This can lead to changes in the amino acid sequence of proteins, potentially altering their function. Understanding substitution is crucial for comprehending how genetic information can be affected and how it relates to DNA repair mechanisms.
Topoisomerases: Topoisomerases are enzymes that play a crucial role in managing DNA supercoiling and torsional strain during processes such as DNA replication and repair. They achieve this by introducing transient breaks in the DNA strands, allowing for the relaxation of supercoiled regions, and then resealing the breaks. This action is essential for maintaining the integrity and accessibility of the DNA during critical cellular functions.
Transition substitution: A transition substitution is a type of point mutation where a purine base is replaced by another purine or a pyrimidine by another pyrimidine. This mutation type affects the DNA sequence but may or may not change the encoded protein.
Transversion substitution: A transversion substitution is a type of point mutation where a purine base is replaced with a pyrimidine base, or vice versa. This mutation can significantly alter the structure and function of DNA.
Uracil: Uracil is a nitrogenous base that is one of the four main building blocks of RNA, replacing thymine found in DNA. It plays a crucial role in coding, decoding, and regulating genes, linking to protein synthesis and various cellular processes.
Xeroderma pigmentosum: Xeroderma pigmentosum (XP) is a rare genetic disorder characterized by an extreme sensitivity to ultraviolet (UV) light, leading to a high risk of skin cancer and other skin abnormalities. This condition arises due to defects in the DNA repair mechanisms, specifically nucleotide excision repair, which is crucial for repairing UV-induced DNA damage. Individuals with XP exhibit symptoms like freckling, sunburn, and skin lesions at a young age due to the inability to effectively repair DNA damage caused by UV radiation.
XPA: XPA is a gene that encodes a protein involved in the nucleotide excision repair (NER) pathway, which is essential for repairing damaged DNA caused by factors like UV radiation and chemical exposure. The XPA protein plays a crucial role in recognizing and verifying DNA damage, thereby facilitating the recruitment of other proteins necessary for the repair process, ensuring genomic stability and preventing mutations.
XPB: XPB is a DNA helicase enzyme that plays a crucial role in nucleotide excision repair (NER), a vital mechanism for repairing DNA damage caused by environmental factors like UV radiation. By unwinding the DNA double helix, XPB allows access to the damaged site, enabling other repair proteins to efficiently remove and replace the defective DNA segments. This function is essential for maintaining genomic stability and preventing mutations that can lead to diseases, including cancer.
XPC: XPC is a protein that plays a crucial role in the DNA repair process, specifically in the recognition of DNA damage and initiating the nucleotide excision repair (NER) pathway. This protein is part of a larger complex that scans the genome for helix-distorting lesions, such as those caused by ultraviolet (UV) light or chemical mutagens. Once XPC identifies damaged DNA, it recruits other proteins to facilitate the repair process, ensuring genomic stability.
XPD: XPD is a protein that plays a critical role in the DNA repair process, specifically in the nucleotide excision repair (NER) pathway. It is part of a larger protein complex that recognizes and removes damaged DNA, particularly from harmful agents like UV light and certain chemicals. The proper functioning of XPD is vital for maintaining genomic stability and preventing mutations that could lead to diseases like cancer.
XPE: XPE, or Xeroderma Pigmentosum Group E, refers to a specific variant of a genetic disorder that affects DNA repair mechanisms, particularly nucleotide excision repair. This condition leads to a heightened sensitivity to ultraviolet (UV) light, resulting in an increased risk of skin cancer and other DNA damage-related conditions. The XPE variant is characterized by a deficiency in the proteins that facilitate the recognition and removal of UV-induced DNA lesions.
XPF: XPF, or Xeroderma Pigmentosum group F, is a crucial protein involved in the nucleotide excision repair (NER) pathway of DNA repair. It plays a vital role in removing damaged DNA caused by ultraviolet (UV) light and other environmental factors, helping maintain genomic stability. By functioning as a DNA damage recognition factor, XPF assists in the repair process, preventing mutations that could lead to various diseases, including cancer.
XPG: XPG is a crucial protein involved in the DNA repair process, specifically in nucleotide excision repair (NER). It functions as a 3' exonuclease, helping to remove damaged DNA segments by cleaving the DNA strand at the site of damage, which is essential for maintaining genomic integrity. XPG plays a key role in recognizing and excising bulky DNA adducts, allowing the repair machinery to restore the DNA to its correct sequence.