BIO 340 Exam 3 Questions And Answers With
Verified Solutions Graded A+ Latest Update 2025.
gene mutation - ANSWER alteration in the DNA sequence, including: single base-pair
substitution (point mutation), insertions or deletions of one or more base pairs, or larger alterations in
chromosome structure
spontaneous mutation - ANSWER changes in the nucleotide sequence with no specific agents
associated with their occurrence- generally assumed to be "accidental"
induced mutation - ANSWER changes in the nucleotide sequence that result from the influence
of external factors of natural or artificial agents, e.g. radiation and chemical agents
transition mutation - ANSWER a point mutation in which a pyrimidine replaces a pyrimidine
(T-C or C-T), or a purine replaces a purine (A-G or G-A)
transversion mutation - ANSWER point mutation in which a pyrimidine replaces a purine (T-A
or G, C-A or G) oor a purine replaces a pyrimidine (A-T or C or G-T or C)
tautomeric shifts - ANSWER mutations resulting in anomalous base-pair relationships (T triple
bonded to G or C double bonded to A) which then in subsequent rounds of DNA replication lead to a
point mutation
photoreactivation - ANSWER utilizes the enzyme, PRE, that searches for DNA dimers and
breaks their covalent bonds. occurs in bacteria only (we have lost the enzyme)
cut and patch repair - ANSWER enzymes constantly surveying DNA for Thymidine dimers, set
of molecules signaled to go in and cut the DNA and pull out a patch of bases including the TT. Patch can
vary 10-100 bases. DNA Poly 1 patches up and fills the gap (mistake-prone) and DNA ligase comes in to
seal the last nick.
Chemical mutations - ANSWER base analogs, chemicals that alter the DNA and intercalating
agents
base analogs - ANSWER compounds that resemble natural bases, but have a high rate of
switching from the common to the rare form. This shift can be mutagenic.
alkylating compounds - ANSWER chemicals cause a reaction that adds either methyl or ethyl
groups to the base. targets G (primarily) or T (secondarily)
imperfect repair - ANSWER base excision, short patch repair, replication error repair
base excision - ANSWER cut out the thymine dimer, leaving just the ribose backbone
replication error repair - ANSWER no damage has occurred, its just that the DNA Poly III put
in the wrong base during replication. This is methyl-directed cut and patch repair. The old/template strand
is methylated so the repair system knows which is the proper strand. This is a long patch repair. Amount
, of DNA excised is ~1000 bases. A completely different set of enzymes are used to cut out the bases when
compared to short patch repair.
error prone repair - ANSWER not template directed. E. coli has 2 polymerases: IV and V
double strand break repair - ANSWER sealing up loose ends of the chromosomes
mutator genes - ANSWER knock out the repair system (mutation in a repair gene)
genes vary mutation rates based on - ANSWER size of the gene
mutation rate - ANSWER # mutations caused - # mutations repaired
computer test - ANSWER tells if your chemical in question structurally resembles known
carcinogens.
Ames test - ANSWER test for mutation by using Salmonella mutant lines and do a reversion
test.
reversion test - ANSWER you have a known mutation in an essential gene in the Salmonella,
add the test solution and screen for reversion to wild type Salmonella.
epidemeology - ANSWER study of disease
cancer - ANSWER accumulation of mutations in a single cell
clonal (re: cancer) - ANSWER set of identical objects; every cell in a tumor is identical and can
be traced back to one single cell that went bad (primary tumor)
mis-regulation - ANSWER divides uncontrollably
no growth control - ANSWER cells are able to go into the cell cycle when they're not supposed
to because the check points (cyclins and CDKs) are no longer regulated.
regulatory genes gone bad - ANSWER truly a genetic disease
loss of contact inhibition - ANSWER your cells are not independent, they are all integrating and
receiving information from neighbors and all over the body (glands making hormones). If you injure a
tissue, the neighbor relationship is lost, and those cells will start growing, restarting the G0 to G1 cell
cycle to heal the wound.
4 non-random factors that cause cancer - ANSWER familial, environmental, viral, sporadic
BRAC-1 - ANSWER gene whose product is used in all cells but when both copies are mutant,
there is an increased likelihood of the person to get breast cancer. does not guarantee that the person will
get breast cancer.
Rb (Retniolblastoma) - ANSWER gene required in all cells. if you inherit one mutant copy,
there is a very good likelihood that you will get retinal cancer, first in one eye, then the other.
familial - ANSWER inherit increased risk of cancer (5%)
environmental - ANSWER cancers of choice (skin cancer, lung cancer) (10%)
viral - ANSWER humans are among the most resistant to viral carcinogenesis. (example of
virus causing cancer in humans is HPV, causes cancer in women.) chickens and cats are highly
Verified Solutions Graded A+ Latest Update 2025.
gene mutation - ANSWER alteration in the DNA sequence, including: single base-pair
substitution (point mutation), insertions or deletions of one or more base pairs, or larger alterations in
chromosome structure
spontaneous mutation - ANSWER changes in the nucleotide sequence with no specific agents
associated with their occurrence- generally assumed to be "accidental"
induced mutation - ANSWER changes in the nucleotide sequence that result from the influence
of external factors of natural or artificial agents, e.g. radiation and chemical agents
transition mutation - ANSWER a point mutation in which a pyrimidine replaces a pyrimidine
(T-C or C-T), or a purine replaces a purine (A-G or G-A)
transversion mutation - ANSWER point mutation in which a pyrimidine replaces a purine (T-A
or G, C-A or G) oor a purine replaces a pyrimidine (A-T or C or G-T or C)
tautomeric shifts - ANSWER mutations resulting in anomalous base-pair relationships (T triple
bonded to G or C double bonded to A) which then in subsequent rounds of DNA replication lead to a
point mutation
photoreactivation - ANSWER utilizes the enzyme, PRE, that searches for DNA dimers and
breaks their covalent bonds. occurs in bacteria only (we have lost the enzyme)
cut and patch repair - ANSWER enzymes constantly surveying DNA for Thymidine dimers, set
of molecules signaled to go in and cut the DNA and pull out a patch of bases including the TT. Patch can
vary 10-100 bases. DNA Poly 1 patches up and fills the gap (mistake-prone) and DNA ligase comes in to
seal the last nick.
Chemical mutations - ANSWER base analogs, chemicals that alter the DNA and intercalating
agents
base analogs - ANSWER compounds that resemble natural bases, but have a high rate of
switching from the common to the rare form. This shift can be mutagenic.
alkylating compounds - ANSWER chemicals cause a reaction that adds either methyl or ethyl
groups to the base. targets G (primarily) or T (secondarily)
imperfect repair - ANSWER base excision, short patch repair, replication error repair
base excision - ANSWER cut out the thymine dimer, leaving just the ribose backbone
replication error repair - ANSWER no damage has occurred, its just that the DNA Poly III put
in the wrong base during replication. This is methyl-directed cut and patch repair. The old/template strand
is methylated so the repair system knows which is the proper strand. This is a long patch repair. Amount
, of DNA excised is ~1000 bases. A completely different set of enzymes are used to cut out the bases when
compared to short patch repair.
error prone repair - ANSWER not template directed. E. coli has 2 polymerases: IV and V
double strand break repair - ANSWER sealing up loose ends of the chromosomes
mutator genes - ANSWER knock out the repair system (mutation in a repair gene)
genes vary mutation rates based on - ANSWER size of the gene
mutation rate - ANSWER # mutations caused - # mutations repaired
computer test - ANSWER tells if your chemical in question structurally resembles known
carcinogens.
Ames test - ANSWER test for mutation by using Salmonella mutant lines and do a reversion
test.
reversion test - ANSWER you have a known mutation in an essential gene in the Salmonella,
add the test solution and screen for reversion to wild type Salmonella.
epidemeology - ANSWER study of disease
cancer - ANSWER accumulation of mutations in a single cell
clonal (re: cancer) - ANSWER set of identical objects; every cell in a tumor is identical and can
be traced back to one single cell that went bad (primary tumor)
mis-regulation - ANSWER divides uncontrollably
no growth control - ANSWER cells are able to go into the cell cycle when they're not supposed
to because the check points (cyclins and CDKs) are no longer regulated.
regulatory genes gone bad - ANSWER truly a genetic disease
loss of contact inhibition - ANSWER your cells are not independent, they are all integrating and
receiving information from neighbors and all over the body (glands making hormones). If you injure a
tissue, the neighbor relationship is lost, and those cells will start growing, restarting the G0 to G1 cell
cycle to heal the wound.
4 non-random factors that cause cancer - ANSWER familial, environmental, viral, sporadic
BRAC-1 - ANSWER gene whose product is used in all cells but when both copies are mutant,
there is an increased likelihood of the person to get breast cancer. does not guarantee that the person will
get breast cancer.
Rb (Retniolblastoma) - ANSWER gene required in all cells. if you inherit one mutant copy,
there is a very good likelihood that you will get retinal cancer, first in one eye, then the other.
familial - ANSWER inherit increased risk of cancer (5%)
environmental - ANSWER cancers of choice (skin cancer, lung cancer) (10%)
viral - ANSWER humans are among the most resistant to viral carcinogenesis. (example of
virus causing cancer in humans is HPV, causes cancer in women.) chickens and cats are highly
