UIowa Human Biology, Exam 2
Questions and Answers
Huge differences in amino acid sequence and protein structure and function.
Enzyme - conservative mutation in active site: - ANSWER-If there is a conservative
mutation in the active site of an enzyme, folding (thus shape) could be only slightly
different than what the protein should normally look like. Still, the substrate that fits in
that enzyme will probably not fit as well, causing the enzyme to catalyze less of the
biochemical reaction than it should.
Channel protein for sucrose - non-conservative mutation in hydrophobic region: -
ANSWER-Non-conservative mutation in a channel protein in the hydrophobic region
of a protein will change the way that it folds, creating new bonds between the new
amino acid and other hydrophilic amino acids in the protein. This will impact if it can
embed in the membrane or impact the channel part of the protein. This will cause
sucrose to not be transport through the channel protein.
Transcription factor - nonsense mutation: - ANSWER-A nonsense mutation early in
the gene thus mRNA transcript will truncate the protein and make it very short. It will
not be able to bind to the sequence of DNA that it recognizes. If it is a TF that
activates a gene, the target gene will not be transcribed.
Why does it make sense that DNA is replicated in a semi-conservative manner? -
ANSWER-It would take too many resources to split the 'old' template strand and new
strand that was made using that strand as a template (because of breaking the
hydrogen bonds). It would also take a lot of carefully monitored mechanisms to re-
attach the two 'old' strands back together and attach the two 'new' strands to each
other after they were made.
How do cells inherit gene expression patterns separate from the information coded in
DNA? - ANSWER-Chromatin patterns - histones & DNA methylation tags -
determine if a gene can be accessed by transcription protein machinery in order to
be expressed/made into a protein.
Describe the 'problem' with lagging strand synthesis. How do telomeres protect
chromosomes against this problem? - ANSWER-After helicase opens up a
replication fork ready for DNA replication, primase creates RNA primers on regions
of DNA using the DNA as a template. This DNA/RNA helix creates a double strand
for DNA polymerase to bind. DNA polymerase can only bind to a double-stranded
nucleic acid. These gaps of RNA in the DNA double helix are eventually filled in with
DNA nucleotides by DNA polymerase.
Two main things create the 'problem' the lagging strand synthesis:
(1) The strands of the DNA double helix are antiparallel (one goes in the 3' 5'
direction and the other in the 5' 3' direction (review DNA structure, nucleotide
constituents, and bonds if this does not make sense).
, (2) DNA polymerase can only read DNA in the 3' 5' direction and synthesize DNA in
the 5' 3' direction
As the lagging strand is synthesized, short fragments (Okazaki fragments) of double
stranded DNA are made as the DNA polymerase moves away from the direction
helicase is opening the DNA. At the end of a strand of DNA, once the RNA
nucleotides are removed from the RNA/DNA helix created by primase there is no
double strand available for DNA polymerase to bind. This single helix at the end of
the chromosome is cleaved to the last base where is a DNA double helix on the
chromosome.
How does telomerase protect against this problem? - ANSWER-Every time a cell
replicates, the chromosome is shortened, the extent to which depends on the cell.
Telomeres are regions of repetitive sequences of DNA that do not code for proteins.
Therefore, as these regions disappear during DNA replication, it does not impact the
function of a cell because no information that codes for a protein is lost. After these
regions get too small the cell will not divide because it cannot pass cell cycle
checkpoints for DNA damage.
After a cell divides, where did the parent cell go? Would you say that it died? -
ANSWER-No it does not die. The original parent cells makes a copy of itself and
after copying itself is still a cell that functions in the body.
What is being checked in the cell checkpoints? Why are these checkpoints
important? - ANSWER-DNA damage, resource availability and cell size to support
more cells, growth cues from other cells, correctly replicated DNA, chromosome
spindle attachment so both cells get the same DNA.
What are 3 reasons for cell death? - ANSWER-Physical damage, viral infections,
radiation, DNA damage, senescence. Getting rid of these cells prevents further DNA
damage that could lead to mutations that promote cancer and reduced function of an
organ or tissue.
Why do you think older animals die of cancer at higher rates than younger animals? -
ANSWER-Since they have been around longer, they have been exposed to more
mutagens, and their cells have had time to acquire more DNA mutations. The more
DNA mutations in a cell, the higher likelihood those mutations can activate genes
that enable cells to grow and divide without regard the organism that it resides in.
Draw a hierarchy of cells in terms of their 'potency', indicate which type of cells they
can become: Embryonic stem cells, adult stem cells, somatic cells. - ANSWER-
Embryonic Stem Cells --> Totipotent, could become any time of cell in the human
body
Adult Stem Cells --> Multipotent, could become a small subset of cells in the human
body (less than the pluripotent germ cells layer stem cells)
Somatic cells --> Not potent, they are differentiated cells that have a specific
function/cell identity.
Questions and Answers
Huge differences in amino acid sequence and protein structure and function.
Enzyme - conservative mutation in active site: - ANSWER-If there is a conservative
mutation in the active site of an enzyme, folding (thus shape) could be only slightly
different than what the protein should normally look like. Still, the substrate that fits in
that enzyme will probably not fit as well, causing the enzyme to catalyze less of the
biochemical reaction than it should.
Channel protein for sucrose - non-conservative mutation in hydrophobic region: -
ANSWER-Non-conservative mutation in a channel protein in the hydrophobic region
of a protein will change the way that it folds, creating new bonds between the new
amino acid and other hydrophilic amino acids in the protein. This will impact if it can
embed in the membrane or impact the channel part of the protein. This will cause
sucrose to not be transport through the channel protein.
Transcription factor - nonsense mutation: - ANSWER-A nonsense mutation early in
the gene thus mRNA transcript will truncate the protein and make it very short. It will
not be able to bind to the sequence of DNA that it recognizes. If it is a TF that
activates a gene, the target gene will not be transcribed.
Why does it make sense that DNA is replicated in a semi-conservative manner? -
ANSWER-It would take too many resources to split the 'old' template strand and new
strand that was made using that strand as a template (because of breaking the
hydrogen bonds). It would also take a lot of carefully monitored mechanisms to re-
attach the two 'old' strands back together and attach the two 'new' strands to each
other after they were made.
How do cells inherit gene expression patterns separate from the information coded in
DNA? - ANSWER-Chromatin patterns - histones & DNA methylation tags -
determine if a gene can be accessed by transcription protein machinery in order to
be expressed/made into a protein.
Describe the 'problem' with lagging strand synthesis. How do telomeres protect
chromosomes against this problem? - ANSWER-After helicase opens up a
replication fork ready for DNA replication, primase creates RNA primers on regions
of DNA using the DNA as a template. This DNA/RNA helix creates a double strand
for DNA polymerase to bind. DNA polymerase can only bind to a double-stranded
nucleic acid. These gaps of RNA in the DNA double helix are eventually filled in with
DNA nucleotides by DNA polymerase.
Two main things create the 'problem' the lagging strand synthesis:
(1) The strands of the DNA double helix are antiparallel (one goes in the 3' 5'
direction and the other in the 5' 3' direction (review DNA structure, nucleotide
constituents, and bonds if this does not make sense).
, (2) DNA polymerase can only read DNA in the 3' 5' direction and synthesize DNA in
the 5' 3' direction
As the lagging strand is synthesized, short fragments (Okazaki fragments) of double
stranded DNA are made as the DNA polymerase moves away from the direction
helicase is opening the DNA. At the end of a strand of DNA, once the RNA
nucleotides are removed from the RNA/DNA helix created by primase there is no
double strand available for DNA polymerase to bind. This single helix at the end of
the chromosome is cleaved to the last base where is a DNA double helix on the
chromosome.
How does telomerase protect against this problem? - ANSWER-Every time a cell
replicates, the chromosome is shortened, the extent to which depends on the cell.
Telomeres are regions of repetitive sequences of DNA that do not code for proteins.
Therefore, as these regions disappear during DNA replication, it does not impact the
function of a cell because no information that codes for a protein is lost. After these
regions get too small the cell will not divide because it cannot pass cell cycle
checkpoints for DNA damage.
After a cell divides, where did the parent cell go? Would you say that it died? -
ANSWER-No it does not die. The original parent cells makes a copy of itself and
after copying itself is still a cell that functions in the body.
What is being checked in the cell checkpoints? Why are these checkpoints
important? - ANSWER-DNA damage, resource availability and cell size to support
more cells, growth cues from other cells, correctly replicated DNA, chromosome
spindle attachment so both cells get the same DNA.
What are 3 reasons for cell death? - ANSWER-Physical damage, viral infections,
radiation, DNA damage, senescence. Getting rid of these cells prevents further DNA
damage that could lead to mutations that promote cancer and reduced function of an
organ or tissue.
Why do you think older animals die of cancer at higher rates than younger animals? -
ANSWER-Since they have been around longer, they have been exposed to more
mutagens, and their cells have had time to acquire more DNA mutations. The more
DNA mutations in a cell, the higher likelihood those mutations can activate genes
that enable cells to grow and divide without regard the organism that it resides in.
Draw a hierarchy of cells in terms of their 'potency', indicate which type of cells they
can become: Embryonic stem cells, adult stem cells, somatic cells. - ANSWER-
Embryonic Stem Cells --> Totipotent, could become any time of cell in the human
body
Adult Stem Cells --> Multipotent, could become a small subset of cells in the human
body (less than the pluripotent germ cells layer stem cells)
Somatic cells --> Not potent, they are differentiated cells that have a specific
function/cell identity.
