Molecular Biology (Lectures 15-17)

Some DNA in Bacteria is methylated. Methylation of DNA helps in the repair of errors during replication. "Old" DNA is methylated (CH3) at A in 5'-GATC-3'. About 10-20 min after replication, before the "new" DNA strand is methylated by "maintenance Methylase", repair systems utilize this "Delay" to select the old/correct strand (methylated) from the new/defective strand (not methylated).

Photolyase is an enzyme that is found in plants, many bacteria, and some animals. It is responsible for repairing thymine dimers directly. Thymine dimers are a type of DNA damage that occurs when two adjacent thymine bases become covalently linked, usually due to exposure to ultraviolet (UV) radiation. Photolyase uses light energy to break the covalent bonds between the thymine bases, restoring the DNA to its original structure. Therefore, photolyase plays a crucial role in maintaining the integrity of DNA and preventing mutations caused by UV radiation.

Base Excision Repair is the correct answer because it is a type of excision repair that specifically fixes a damaged, single base. In this repair mechanism, the damaged base is excised by a specific DNA glycosylase enzyme, creating an apurinic/apyrimidinic (AP) site. The AP site is then recognized and processed by other enzymes, resulting in the removal and replacement of the damaged base with the correct one. This repair pathway is important for maintaining the integrity of the DNA molecule and preventing the accumulation of mutations.

The correct answer is nucleotide excision repair. This repair system is responsible for managing thymine dimers in humans. Thymine dimers are formed when two adjacent thymine bases in DNA become covalently bonded, usually as a result of exposure to UV radiation. Nucleotide excision repair involves the removal and replacement of the damaged DNA segment to restore the integrity of the DNA molecule. This process is essential for maintaining the stability and function of the genome.

DNA Microarray is the process in which fragments of DNA from each gene are "spotted" and immobilized on a glass microscope slide. This technique allows scientists to study the expression levels of thousands of genes simultaneously, providing valuable information about gene function and regulation. By hybridizing labeled DNA samples to the immobilized DNA fragments, researchers can determine which genes are active or turned on in a particular cell or tissue type. This technology has revolutionized the field of genomics and has applications in various areas of biological research and medicine.

Photolyase is a protein that repairs DNA damage caused by exposure to ultraviolet (UV) light. It is induced by light, specifically by the absorption of photons in the visible light spectrum. When photolyase absorbs light, it undergoes a chemical reaction that enables it to repair the UV-induced DNA damage. Therefore, the presence of light is necessary to activate and induce the function of photolyase in repairing DNA.

Alkylation refers to the process of adding an alkyl group to a molecule. In this case, the point mutation adds a C-H alkyl group to either N or O atoms. Alkylation can occur through various mechanisms, such as the substitution of a hydrogen atom with an alkyl group. This process can have significant effects on the properties and reactivity of the molecule, leading to changes in its function or behavior. The term "alkylation" can be written in both uppercase and lowercase letters.

The given answer "SOS" is the correct explanation for the inducible repair system in E. coli. SOS is a response system that is activated in E. coli when the DNA is damaged by mutagenic stress or the formation of T-dimers. This system triggers a series of DNA repair mechanisms to fix the damage and restore the integrity of the DNA. The SOS response involves the activation of various genes that are responsible for DNA repair, replication, and mutagenesis. Overall, SOS is an important mechanism that allows E. coli to survive and adapt to DNA damage.

Thymine dimers are formed when UV light causes two adjacent thymine bases on a DNA strand to bond together, forming a dimer. This type of point mutation can lead to DNA damage and disrupt normal DNA replication and transcription processes. Thymine dimers are particularly common in individuals with prolonged exposure to UV radiation, such as those who frequently spend time in the sun without protection.

Both types of NER, Nucleotide Excision and nucleotide excision, activate the same repair proteins. This suggests that regardless of the capitalization of the term, the two types of NER refer to the same process and involve the same repair proteins.

Heteroduplex DNA refers to a DNA molecule that is formed when two complementary strands with non-pairing bases come together. In E.coli, the process involves mut genes, while in eukaryotes, it involves msh genes (mutS homologes). The term "heteroduplex DNA" is used to describe this specific type of DNA structure.

The given answer options all refer to the same concept, which is replication errors. Replication errors occur when incorrect bases are added by DNA polymerase during DNA replication. These errors are not corrected by the 3'-5' exonuclease proofreading mechanism. The two categories of replication errors mentioned are "transversion" and "transition" mutations.

People with Xeroderma Pigmentosum (XP) have defective NER systems, which is caused by at least eight different genes for NER. Xeroderma Pigmentosum is a rare genetic disorder that affects the body's ability to repair damage caused by ultraviolet (UV) light. This leads to extreme sensitivity to sunlight, increased risk of skin cancer, and other symptoms such as freckling and pigment changes. The defective NER systems in individuals with XP prevent the proper repair of DNA damage caused by UV light, making them more susceptible to the harmful effects of sunlight.

Excision repair systems are mechanisms that repair DNA damage, including mutations. They are known to repair the majority of mutations, making the first statement true. Additionally, there are multiple redundant types of excision repair systems, which means that there are different pathways or mechanisms that can perform the repair process. This makes the second statement true. Furthermore, each type of excision repair system deals with different kinds of point mutations, indicating that they have specific functions and targets in repairing DNA damage. This makes the last statement true as well.

The two types of NER forms in Eukaryotes are Global Genome NER and Transcribed Strands NER. These processes are responsible for repairing DNA damage in different regions of the genome. Global Genome NER repairs damage throughout the entire genome, while Transcribed Strands NER specifically repairs damage in the transcribed regions of the genome where active genes are located. Both forms of NER are important for maintaining the integrity of the DNA and preventing mutations that can lead to diseases such as cancer.

Base excision repair is a DNA repair mechanism that corrects small, non-bulky lesions in the DNA, such as damaged bases. It involves the removal of the damaged base by specific enzymes called DNA glycosylases. These enzymes recognize and cleave the glycosidic bond between the damaged base and the sugar-phosphate backbone. Once the damaged base is removed, the resulting gap in the DNA is filled in with the correct nucleotide sequence by DNA polymerase and sealed by DNA ligase. Therefore, base excision repair performs by removing the damaged base and replacing it with the correct nucleotide.

Nucleotide excision repair (NER) is a DNA repair mechanism that fixes damaged bases. It involves the removal of a stretch of 10-12 nucleotides surrounding the damaged site. The repair process also involves the participation of uvr genes, which are responsible for encoding proteins involved in NER. Therefore, the given answer correctly states that NER fixes damaged bases, removes 10-12 nucleotides, and involves uvr genes.

Xeroderma Pigmentosum (XP) is a genetic disorder that affects the ability of cells to repair DNA damage caused by ultraviolet (UV) radiation. Individuals with XP cannot repair bulky DNA damage such as T-dimers and abasic sites. This makes them more susceptible to developing skin cancer, with a risk that is 1000 times higher than the general population. Exposure to sunlight, which contains UV radiation, further increases the risk of cancer in people with XP, particularly in relation to T-dimers.

The mismatch repair system is responsible for fixing mismatches that occur during DNA replication. This system identifies and removes the incorrect base pairs and replaces them with the correct ones. It plays a crucial role in maintaining the accuracy of DNA replication and preventing mutations.

p53 is a transcription factor that activates cell cycle control, DNA repair, and apoptosis.

Non-Homologous End Joining (NHEJ) is a DNA repair system that "ligates" or joins together the ends of broken linear DNA, such as chromosomes. It is particularly important for repairing DNA breakage caused by ionizing radiation. NHEJ does not require a homologous template for repair, hence the term "non-homologous" in its name. This process is essential for maintaining genomic stability and preventing the accumulation of DNA damage.

The correct answer is Methylation. Methylation of bases provides cues as to which strand is correct. Methylation is a process where a methyl group is added to a DNA molecule, and it plays a role in DNA repair. In this case, the correct strand is the one that is methylated, indicating that it is the correct version without the mutated base. The other strand, which is not methylated, has the mutated base.

Depurination is a process in which purine bases are removed from DNA, forming abasic sites. The frequency at which this process occurs is roughly 10000 purines per cell per day. This means that approximately 10000 purine bases are removed from DNA in a single cell in a day. The answer provided states this information correctly, mentioning both the process (depurination) and the frequency (10000).

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The correct answer is mutagenic stress, umu, RecA, LexA. The inducible repair SOS system in E. coli is activated by DNA damage, specifically mutagenic stress. This activation leads to an increase in the expression of umu genes, which are involved in error-prone bypass repair mechanisms. The induction of the SOS system involves RecA, which acts as a protease to destroy LexA, a transcription inhibitor. This allows for the expression of genes involved in DNA repair and mutagenesis.