Chapter 7
Rate of spontaneous mutation during replication for most organisms
1/10^9 base pairs
(BLANK) enzymes can remove them so as to re-create the original base.
alkyltransferase
base analogs can cause
base substitutions on the complementary strand synthesized in the next round of DNA replication
1st step of Base Excision Repair
deaminated DNA with uracil
mutagens that are intercalcators
flat, planar molecules that can sandwich themselves between successive base pairs and disrupt the machinery for replication, generating deletions or insertions of a single base pair
1st step of mismatch repair
parental strands are marked with methyl groups
the enzyme (BLANK) recognizes the thymine dimers produced by exposure to ultraviolet light
photolyase
2nd step of mismatch repair
proteins MutS and MutL recognize mismatch in the replicated DNA
3rd step of Base Excision Repair
AP endonuclease cuts backbone to make a nick at the AP site
base excision repair
enzymes called DNA glycosylases cleave an altered nitrogenous base from the sugar of its nucleotide, releasing the base and creating an apurinic or apyrimidinic (AP) site in the DNA chain
mutation hotspot
region of a gene that is prone to mutation
during replication, proflavin causes
single base insertions and deletions
Deamination causes what kinds of mutations?
transition mutations
a mutagen is
A chemical or physical agent that interacts with DNA and causes a mutation.
forward mutation
Changes the wild-type phenotype to a mutant phenotype
4th step of mismatch repair
DNA exonucleases excise DNA from unmethylated new strand
4th step of Base Excision Repair
DNA exonucleases remove the nucleotides near the nick, creating a gap
6th step of Base Excision Repair
DNA ligase seals the gap
5th step of Base Excision Repair
DNA polymerase synthesizes new DNA to fill in the gap
2nd step of Base Excision Repair
Glycosylase removes uracil, leaving an AP site
Complementation
If two homologous chromosomes in an individual each carry a mutation recessive to wild type, that individual will have a normal phenotype if the mutations are in different genes.
3rd step of mismatch repair
MutL recruits MutH to GATC; MutH makes a nick in strand opposite methyl tag
hydroxylating agents
add -OH groups to DNA bases
alkylating agents
add ethyl (-CH2-CH3) or methyl (-CH3) groups to DNA bases
a mutation is
an inherited change in the sequence of the genetic material
Mutations in somatic cells (BLANK) heritable. Mutations in germ cells (BLANK) heritable.
are not, are
mutagens that are base analogs
are so similar in chemical structure to the normal nitrogenous bases that the replication machinery can incorporate them into DNA
substitution mutation
change of one base to one of the other 3 bases
deamination leads to a type of DNA damage that converts cytosine to uracil which
changes a C-G base pair to T-A in replication.
three types of mutagens that directly alter a base's chemical structure + properties
deaminating agents, hydroxylating agents, alkylating agents
genes encode for
enzymes, protein hormones, receptor proteins, proteins that support chromosomes, proteins that provide cell shape
mismatch repair corrects
errors in DNA replication
UV light causes the
formation of thymine dimers in DNA
proflavin is an
intercalcating agent
ames test tests for
mutagenicity
reversion mutation
mutant phenotype to wild type phenotype
deaminating agents
remove -NH2 groups from DNA bases
nucleotide excision repair
removes alterations that base excision cannot repair because the cell lacks a DNA glycosylase that recognizes the problem base(s).
5th step of mismatch repair
repair and methylation of newly synthesized DNA strand
tautomerization
temporary change in DNA base structure due to the movement of H atoms
unstable trinucleotide repeats are repeated sequences of 3 bases
that can increase or decrease in number generation after generation
Depurination
the loss of a purine base from a nucleotide
deamination
the removal of an amino group from an amino acid