WGU 785 Final
Exam
1. Hemophilia Pedigree - Father has hemophilia, mother does not. What is the outcome for their kids?: His
daughters would be carriers. This is x-link recessive.
2. Autosomal:
Dominant:: Autosomal: males and females equally affected. Dominant: non-carrier parents
3. polymerase chain reaction (PCR): The process of copying DNA in the lab. Uses Template DNA, Nucleotides
(dNTPS), DNA Polymerase, and DNA primers.
4. 3 Steps of PCR: 1. Denaturation: DNA is heated to 95C to separate it.
2. Annealing: reaction is cooled to 50C; primers stick to the DNA you want to copy and add DNA polymerase.
3. Elongation: reaction heated to 70C and DNA polymerase, adding nucleotides building a new DNA strand.
5. Base Excision Repair (BER): How you repair a mutation. BER is used to repair damage to a base caused by
harmful molecules. You remove the base that is damaged and replace it. *BER removes a single nucleotide*
DNA glycolsylase - sees damaged DNA and removes it.
DNA polymerase-puts the right one back in while DNA ligase seals it.
6. Mismatch repair (MMR) occurs during:: replication. DNA polymerase proof- reads but sometimes a mismatch
pair gets through. MMR removes a large section of the nucleotides from the new DNA and DNA polymerase tries
again. (Ex: C-T instead of C-A)
7. Mismatch Repair corrects what kind of DNA damage?: When a base is mis- matched due to errors in replication.
Such as G-T instead of G-C. DNA polymerase comes by and fixes it.
8. What happens when DNA polymerase binds to DNA to make RNA?: TRAN- SCRIPTION! DNA polymerase
takes the individual nucleotides and matches them to the parental sequences to ensure a correct pair. It must bind with
RNA primer to work.
9. What is needed for DNA replication?: DNA polymerase
10.Nonsense Mutation: Change in 1 nucleotide produces a STOP codon Stop= nonsense because it is no more.
11.Silent Mutation: Change in 1 nucleotide but codes for the same amino acid. Silent= the change doesn't change
the name of the protein
12. Missense Mutation: Change in 1 nucleotide leads to a code for a different amino acid. Missense = mistake
was made.
13.What happends during RNA splicing?: During RNA splicing introns are cut out, the remaining exons are
joined together.
14.5'ATG AGT CTC TCT 3'
Find the DNA template strand.: 3'TAC TCA GAG AGA 5'
, WGU 785 Final
Exam
The DNA template strand is complimentary. So start with the opposite number, then go L-R with the complimentary lette
15.5'ATG AGT CTC TCT 3'
What is the corresonding mRNA sequence?: 5'AUG AGU CUC UCU 3'
This sequence is the same as the coding strand except T changes to U because it is RNA. RNA doesn't have T.
16.How would a mutation from CTC to ATC affect the protein sequence? (CTC/ATC - coding strand, AUC -
mRNA strand): This will make a missense mutation because it changes the name of the protein. (look at the chart
provided.) missense = mistake
17.DNA replication process: DNA ->Transcription -> RNA -> Translation -> Polypeptide
18.Describe how you would find what ionized Alanine looks like.: This is an amino acid. Look for the "R"
group. Alanine is a hydrophobic amino acid that has CH3. It is a weak interaction. An ionized acid will have a + or -
charge.
19.Describe what causes the misfolding of protein in Alzheimer's Disease.: - Protein misfolding is caused by
intracellular tangles and extracellular plaques (senile plaques) caused by abnormal protein aggregation.
TAU is fibrous material inside cells where the connections are lost. This becomes defective and forms filaments in the
neuron.
Amyloid-Beta is a large precursor protein in the cell. Excess amyloid-beta creates senile plaques. This starts in the
hippocampus and moves up.
20.Describe the process of neurodegenerative protein aggregation.: - Alzheimer's is the most common
neurodegenerative disease. The formation of aggregated amyloid-beta fibers is another characterisitc of Alzheimer's.
However, neurodegeneration and memory loss can be detected before amyloid fibers accu- mulate in the brain.
21.What are the molecules that help denatured proteins with folding?: Mol- ecular chaperones are protein helpers.
They bind to the newly made polypeptide and enable proper folding. Proper protein folding is vital b/c proteins that do
not fold properly can lead to a variety of diseases. Normally, the chaperones that help new proteins fold can also help
misfolded proteins refold into the correct structure. Genetic mutations that substitute one amino acid for another can
cause incorrect folding.
22.What are the 4 levels of protein structure?: 1. Primary-chain of amino acids. PEPTIDE bonds form a
polypeptide chain. This is a covalent bond (very strong) and does not denature.
2. Secondary-alpha helix and beta sheet. HYDROGEN bonds that contain the carboxyl group and amino groups.
Denatured by salt and pH change.
Exam
1. Hemophilia Pedigree - Father has hemophilia, mother does not. What is the outcome for their kids?: His
daughters would be carriers. This is x-link recessive.
2. Autosomal:
Dominant:: Autosomal: males and females equally affected. Dominant: non-carrier parents
3. polymerase chain reaction (PCR): The process of copying DNA in the lab. Uses Template DNA, Nucleotides
(dNTPS), DNA Polymerase, and DNA primers.
4. 3 Steps of PCR: 1. Denaturation: DNA is heated to 95C to separate it.
2. Annealing: reaction is cooled to 50C; primers stick to the DNA you want to copy and add DNA polymerase.
3. Elongation: reaction heated to 70C and DNA polymerase, adding nucleotides building a new DNA strand.
5. Base Excision Repair (BER): How you repair a mutation. BER is used to repair damage to a base caused by
harmful molecules. You remove the base that is damaged and replace it. *BER removes a single nucleotide*
DNA glycolsylase - sees damaged DNA and removes it.
DNA polymerase-puts the right one back in while DNA ligase seals it.
6. Mismatch repair (MMR) occurs during:: replication. DNA polymerase proof- reads but sometimes a mismatch
pair gets through. MMR removes a large section of the nucleotides from the new DNA and DNA polymerase tries
again. (Ex: C-T instead of C-A)
7. Mismatch Repair corrects what kind of DNA damage?: When a base is mis- matched due to errors in replication.
Such as G-T instead of G-C. DNA polymerase comes by and fixes it.
8. What happens when DNA polymerase binds to DNA to make RNA?: TRAN- SCRIPTION! DNA polymerase
takes the individual nucleotides and matches them to the parental sequences to ensure a correct pair. It must bind with
RNA primer to work.
9. What is needed for DNA replication?: DNA polymerase
10.Nonsense Mutation: Change in 1 nucleotide produces a STOP codon Stop= nonsense because it is no more.
11.Silent Mutation: Change in 1 nucleotide but codes for the same amino acid. Silent= the change doesn't change
the name of the protein
12. Missense Mutation: Change in 1 nucleotide leads to a code for a different amino acid. Missense = mistake
was made.
13.What happends during RNA splicing?: During RNA splicing introns are cut out, the remaining exons are
joined together.
14.5'ATG AGT CTC TCT 3'
Find the DNA template strand.: 3'TAC TCA GAG AGA 5'
, WGU 785 Final
Exam
The DNA template strand is complimentary. So start with the opposite number, then go L-R with the complimentary lette
15.5'ATG AGT CTC TCT 3'
What is the corresonding mRNA sequence?: 5'AUG AGU CUC UCU 3'
This sequence is the same as the coding strand except T changes to U because it is RNA. RNA doesn't have T.
16.How would a mutation from CTC to ATC affect the protein sequence? (CTC/ATC - coding strand, AUC -
mRNA strand): This will make a missense mutation because it changes the name of the protein. (look at the chart
provided.) missense = mistake
17.DNA replication process: DNA ->Transcription -> RNA -> Translation -> Polypeptide
18.Describe how you would find what ionized Alanine looks like.: This is an amino acid. Look for the "R"
group. Alanine is a hydrophobic amino acid that has CH3. It is a weak interaction. An ionized acid will have a + or -
charge.
19.Describe what causes the misfolding of protein in Alzheimer's Disease.: - Protein misfolding is caused by
intracellular tangles and extracellular plaques (senile plaques) caused by abnormal protein aggregation.
TAU is fibrous material inside cells where the connections are lost. This becomes defective and forms filaments in the
neuron.
Amyloid-Beta is a large precursor protein in the cell. Excess amyloid-beta creates senile plaques. This starts in the
hippocampus and moves up.
20.Describe the process of neurodegenerative protein aggregation.: - Alzheimer's is the most common
neurodegenerative disease. The formation of aggregated amyloid-beta fibers is another characterisitc of Alzheimer's.
However, neurodegeneration and memory loss can be detected before amyloid fibers accu- mulate in the brain.
21.What are the molecules that help denatured proteins with folding?: Mol- ecular chaperones are protein helpers.
They bind to the newly made polypeptide and enable proper folding. Proper protein folding is vital b/c proteins that do
not fold properly can lead to a variety of diseases. Normally, the chaperones that help new proteins fold can also help
misfolded proteins refold into the correct structure. Genetic mutations that substitute one amino acid for another can
cause incorrect folding.
22.What are the 4 levels of protein structure?: 1. Primary-chain of amino acids. PEPTIDE bonds form a
polypeptide chain. This is a covalent bond (very strong) and does not denature.
2. Secondary-alpha helix and beta sheet. HYDROGEN bonds that contain the carboxyl group and amino groups.
Denatured by salt and pH change.
