A type of point mutation where T changes to C or A changes to G.
Base excision repair, nonhomologous end joining, and homologous recombination.
DNA polymerase β.
It binds to a mispaired segment of DNA and distinguishes between the template and the newly synthesized daughter strand.
An endonuclease that cuts the newly synthesized daughter strand.
18,000 depurination events.
Mutations that change a single base or base pair.
It flips the thymine base out of the helix and cuts it off the sugar-phosphate DNA backbone.
It unwinds the DNA helix.
Human cells.
Cancers.
8-oxoG.
XP-G and RPA proteins.
It is degraded to mononucleotides.
100 cytosine deamination events.
A half-opened right hand.
A process that can lead to DNA mutations.
APE1 cuts the DNA backbone at the abasic site.
DNA ligase links the inserted base to the backbone.
Double-helix distortion caused by T-T dimers.
DNA regions containing chemically modified bases (chemical adducts) that distort the normal shape of DNA.
Mutations in any of at least seven different genes, called XP-A through XP-G.
A bubble of about 25 bases in the DNA.
It removes several nucleotides from the cut end of the daughter strand, including the mismatched base.
A T·G mismatch.
An apurinic site.
They recognize and repair damage in DNA.
Just the deoxyribose phosphate.
DNA Pol β inserts the single base.
It recruits the transcription factor TFIIH.
Increased risk of cancer and other diseases.
Deamination of C to U or 5-methyl C to T.
It can lead to uncontrolled cell growth and tumor formation.
Nucleotide excision repair.
It repairs damage and copying errors.
Mutations caused by insertions or deletions that alter the reading frame of the gene.
Mutations that create a premature stop codon in the protein sequence.
Errors introduced during replication.
Replication errors.
By the 3’ to 5’ exonuclease activity (proofreading) of DNA Polymerase.
The binding of MSH2 - MSH6.
They act as endonucleases to cut out the damaged strand.
To remove the mismatched T and replace it with a C.
Base excision repair.
T·G mismatches.
They halt cell replication, potentially leading to cell death.
C – C bonds, resulting in thymine-thymine dimers.
Byproducts of metabolism that can cause DNA mutations.
Approximately 30 proteins.
Copying errors and the effects of various physical and chemical agents.
It removes the deoxyribose phosphate.
N-glycosidic bond.
They partially unwind the double helix using ATP.
Spontaneous DNA damage.
Mutations where T <-> G/A and A <-> C/T.
At least seven different genes (XP-A through XP-G).
DNA damage, which is a change in the normal DNA sequence.
It causes melting of the newly formed end and polymerase pausing.
External factors like carcinogens and radiation.
A T·G mismatch.
It recognizes double-helix distortion, such as that caused by a T-T dimer.
Nucleotide excision repair.
It is unclear how the MSH2-MSH6 complex distinguishes between strands, possibly related to the status of the 3’ end of the daughter strand.
A point mutation that changes the protein amino acid sequence.
Oxidation.
Point mutations.
The 'fingers'.
A type of DNA damage that can result in mutations.
DNA polymerase.
It affects base pairing during the next round of DNA replication.
A condition where the genetic information of a cell is prone to mutations and alterations.
Adenine and guanine.
Adenine (A).
They are components of the nucleotide excision-repair system that, when mutated, cause sensitivity to UV.
They often lead to deamination.
Mutations that do not change the amino acid sequence of a protein.
Mismatch excision repair.
A T·G mismatch.
The daughter strand is transiently uniquely methylated.
A point mutation that introduces a stop codon.
Depurination.
The normal C·G base pair will become a T·A mutation during replication.
T - T dimers.
Coding regions contain sequences that are translated into proteins, while non-coding regions do not.
Mistakes during DNA replication.
UV rays from sunlight.
Errors in DNA replication, damage from environmental factors, and defects in DNA repair mechanisms.
Deamination of 5-Methylcytosine (C) to thymine (T).
Yes, other glycosylases are specific for different base modifications.
They generate a kink in the helix.
Spontaneous cleavage of bonds.
It connects the new section of DNA to the backbone.
DNA ligase.
24 – 32 bases apart on each side of the lesion.
They correct errors in DNA to maintain genetic integrity.
Mutations that involve a change in a single nucleotide.
In the junction between the fingers and the palm.
It flips back into the polymerase site and elongation resumes.
Xeroderma pigmentosum.
A point mutation that may not change the amino acid sequence, often occurring in the third codon position.
It can change gene expression.
Pyrimidine dimers.
Point mutations where T changes to G/A, A changes to C/T, or C changes to A/G, and G changes to C/T.
The mispaired base and probably other bases are removed.
They are substances that can cause DNA mutations.
It fills the gap in the DNA strand.
Inheritable loss-of-function mutations in MSH2 or MLH1.
Mutations that result in a change in one amino acid in the protein sequence.
They can cause DNA damage leading to mutations.
Melanomas and squamous cell carcinomas.
