Chapter 15

Question 1

List several ways that mutations can alter the amino acid sequence of a polypeptide

Answer 1

Mutations can alter the amino acid sequence of a polypeptide in several ways:

Silent Mutation: One type of base is replaced by a different base; the new codon specifies the same amino acid; it causes no change in the protein function
Missense Mutation: One type of base is replaced by a different base; the new codon specifies a different amino acid; this usually has a neutral or negative outcome
Nonsense Mutation: One type of base is replaced by a different base; the new codon specifies a stop codon- causes early stop to translation and a shortened protein; this usually has a negative outcome
Frameshift Mutation: One type of base is inserted or deleted; it changes the reading frame; changes the amino acid after deletion/addition; changes protein structure and function and usually has a negative outcome

Question 2

Describe examples of how mutations can cause human genetic diseases

Answer 2

Mutations in DNA can lead to a variety of genetic disorders. Here are some examples:

Sickle Cell Disease: This is a group of disorders that affects hemoglobin, the molecule in red blood cells that delivers oxygen to cells throughout the body. It is caused by a mutation in the HBB gene

Cystic Fibrosis: This is a progressive, genetic disease that causes persistent lung infections and limits the ability to breathe over time. It is caused by mutations in the CFTR gene

Question 3

Compare and contrast the effects of mutations in somatic cells versus germ-line cells

Answer 3

Mutations can occur in both somatic cells and germ-line cells, and the effects of these mutations can vary significantly:

Somatic Cells:
Somatic mutations are changes to a person’s DNA that occur after conception in any cell that isn’t a germ cell (egg or sperm cell)
These mutations do not pass from parents to their children (not hereditary) and happen sporadically or randomly, without the mutation existing in a person’s family history
They also can’t pass to future generations
Changes made to somatic cells affect that person’s body alone
While somatic gene editing affects only the patient being treated (and only some of his or her cells), the possible consequences of that are difficult to predict

Germ-line Cells:
Germline mutations occur in a parent’s reproductive cells (egg or sperm). These mutations change the genetic material that the child receives from their parent (hereditary)
You can inherit germline mutations from either parent
Any alterations made to them will be passed from parent to child—affecting all future generations

Question 4

Discuss the common types of DNA repair systems and list their general features

Answer 4

DNA repair systems are crucial for maintaining the integrity of the genetic material in cells. They correct errors that occur during DNA replication and repair damage caused by various factors. Here are some common types of DNA repair systems and their general features:

Direct Reversal Repair: This mechanism directly reverses the damage without removing the base1. It’s a simple and efficient way to correct certain types of DNA damage

Base Excision Repair (BER): This mechanism is used to fix small, non-helix-distorting base lesions, most commonly caused by oxidation or alkylation. It involves the removal of the damaged base, followed by the insertion of a correct base

Nucleotide Excision Repair (NER): This mechanism repairs bulky, helix-distorting lesions, such as those caused by ultraviolet light-induced pyrimidine dimers. It involves the removal of a short single-strand DNA segment that includes the lesion, followed by DNA synthesis to fill the gap

Question 5

Outline the steps in the development of cancer

Answer 5

The development of cancer is a multi-step process that involves mutation and selection for cells with progressively increasing capacity for proliferation, survival, invasion, and metastasis. Here are the general steps in the development of cancer:

Initiation: This is the stage where a carcinogen enters the body and is transported into cells. Carcinogens cause cancer by permanently damaging a cell’s DNA, mutating it from a normal cell to a cancer cell. The cancer cell then replicates, and the cancer may spread to other tissues and body systems

Promotion: In this stage, the cells continue to divide, impacting nearby normal cells, often reducing the function of the affected organ. As the cells become more abnormal, they gain new capabilities, such as the ability to release growth factors and digestive enzymes

Progression: This is the final stage of cancer development where the cells gain a progressively increasing capacity for proliferation, survival, invasion, and metastasis. The cells continue to divide and grow, often reducing the function of the affected organ

Question 6

Describe the function of proto-oncogenes and the mutated form, oncogenes

Answer 6

Proto-oncogenes are healthy genes found in cells that are responsible for making proteins involved in cell growth, division, and other processes. They contain the necessary information for your body to make the proteins responsible for stimulating cell division, inhibiting cell differentiation, and preventing apoptosis, also known as cell death. These processes are all essential for cells to maintain healthy tissues and organs in your body

However, if an error (mutation) occurs in a proto-oncogene, the gene can become turned on when it isn’t supposed to be. If this happens, the proto-oncogene can turn into a malfunctioning gene called an oncogene. Cells will start to grow out of control, which leads to cancer. Oncogenes can replicate continuously, becoming out of control. They can mutate and permanently activate as oncogenes

Question 7

Identify the two general functions of the proteins encoded by tumor-suppressor genes

Answer 7

Tumor suppressor genes encode proteins that have two general functions:

Regulation of Cell Division: Tumor suppressor genes help regulate a complicated cellular timetable, sometimes called the cell cycle. They keep cells from dividing too fast and multiplying so quickly that they form tumors. They make sure cells, which typically live for a set time, only live as long as they’re supposed to live. This is “programmed” cell death (apoptosis)

DNA Damage Repair: Tumor suppressor genes repair DNA damage that can happen when cells divide more quickly than usual. They act to regulate cell division, keeping it in check. When a tumor suppressor gene is inactivated by a mutation, the protein it encodes does not function properly, and as a result, uncontrolled cell division may occur. Such mutations may contribute to the development of a cancer

Question 8

Mutation

Answer 8

A mutation is a change in the DNA sequence of an organism. Mutations can result from errors in DNA replication during cell division, exposure to mutagens, or a viral infection. Germline mutations (that occur in eggs and sperm) can be passed on to offspring, while somatic mutations (that occur in body cells) are not passed on

Question 9

Allele

Answer 9

An allele is a variant form of a gene. Some genes have a variety of different forms, which are located at the same position, or genetic locus, on a chromosome. Humans are called diploid organisms because they have two alleles at each genetic locus, with one allele inherited from each parent. If the two alleles are the same, the individual is homozygous for that allele. If the alleles are different, the individual is heterozygous. The specific version of each gene that a parent passes down to their child is known as an allele. Alleles influence the way our body’s cells work, determining traits and characteristics like skin pigmentation, hair and eye color, height, blood type, and much more

Question 10

Single Nucleotide

Answer 10

A single nucleotide is the basic building block of nucleic acids, which include RNA and DNA. Each nucleotide is made up of three parts: a nitrogen-containing ring structure called a nitrogenous base, a five-carbon sugar, and at least one phosphate group

In the context of genetics, a single nucleotide polymorphism (SNP) is a germline substitution of a single nucleotide at a specific position in the genome that is present in a sufficiently large fraction of considered population. For example, a G nucleotide present at a specific location in a reference genome may be replaced by an A in a minority of individuals. The two possible nucleotide variations of this SNP – G or A – are called alleles

Question 11

Polymorphism

Answer 11

Polymorphism, in the context of genetics, refers to the presence of two or more variant forms of a specific DNA sequence that can occur among different individuals or populations. The most common type of polymorphism involves variation at a single nucleotide, also called a single-nucleotide polymorphism, or SNP

Question 12

Homozygous vs Heterozygous

Answer 12

Homozygous and heterozygous are terms used in genetics to describe the pairs of genes you inherit from your parents

If you are homozygous for a particular gene, it means you inherited the same version of that gene from both your mother and father. For example, if you inherited the gene for blonde hair from both your parents, you are homozygous for the gene that controls hair color

On the other hand, if you are heterozygous for a particular gene, it means you inherited two different versions of the gene, one from your mother and one from your father. For instance, if you inherited the gene for blonde hair from your mother and the gene for brown hair from your father, you are heterozygous

Question 13

Synonymous Substitution

Answer 13

A synonymous substitution, often called a silent substitution, is the evolutionary substitution of one base for another in an exon of a gene coding for a protein, such that the produced amino acid sequence is not modified. This is possible because the genetic code is “degenerate”, meaning that some amino acids are coded for by more than one three-base-pair codon

Question 14

Silent Substitution

Answer 14

A silent substitution, often called a silent mutation, is the evolutionary substitution of one base for another in an exon of a gene coding for a protein, such that the produced amino acid sequence is not modified. This is possible because the genetic code is “degenerate”, meaning that some amino acids are coded for by more than one three-base-pair codon

Question 15

Nonsynonymous substitution

Answer 15

A nonsynonymous substitution is a type of mutation in which a change in the nucleotide sequence of a gene results in a different amino acid being incorporated during the translation of that gene. This is different from a synonymous substitution, which does not alter the amino acid sequence

Nonsynonymous substitutions can lead to changes in the protein produced, potentially altering its function. These substitutions can be further classified as conservative (a change to an amino acid with similar physiochemical properties), semi-conservative (e.g., a change from a negatively to positively charged amino acid), or radical (a change to a vastly different amino acid)

Examples:
Missense mutations
Nonsense mutations

Question 16

Missense

Answer 16

These are nonsynonymous substitutions that arise from point mutations, mutations in a single nucleotide that result in the substitution of a different amino acid, resulting in a change to the protein encoded. Some missense mutations can alter the function of the resulting protein. However, not all missense mutations lead to significant protein changes.

Question 17

Nonsense

Answer 17

These are nonsynonymous substitutions that result in a premature stop codon, leading to a truncated protein.

A nonsense mutation is a type of point mutation that results in a premature stop codon, or a nonsense codon, in the transcribed mRNA, and possibly a truncated, and often nonfunctional, protein product. This occurs when a sequence change in the DNA gives rise to a stop codon rather than a codon specifying an amino acid

Question 18

Frameshift

Answer 18

A frameshift mutation is a type of gene mutation in which the addition or deletion of one or more nucleotides causes a shift in the reading frame of the codons in the mRNA. This can lead to the alteration in the amino acid sequence at protein translation

Frameshift mutations are insertions or deletions in the genome that are not in multiples of three nucleotides

Question 19

Translocation

Answer 19

A translocation, in genetics, is a type of chromosomal abnormality where a chromosome breaks and a portion of it reattaches to a different chromosome. This mixing of genetic material can lead to important results. The resultant chromosomes may lack some genetic information and have excessive amounts of some. Many important clinical conditions like Down syndrome and chronic myelogenous leukemia result from translocation mutations

Question 20

Inversion

Answer 20

An inversion is a type of chromosomal rearrangement in which a segment of a chromosome becomes inverted within its original position. This occurs when a chromosome undergoes two breaks within the chromosomal arm, and the segment between the two breaks inserts itself in the opposite direction in the same chromosome arm. The number of genes captured by an inversion can range from a handful of genes to hundreds of genes

Question 21

Post-replication mismatch repair

Answer 21

Post-replication mismatch repair is a type of DNA repair mechanism that occurs after DNA replication. It is designed to fix any errors that were not corrected during the replication process

During DNA replication, most DNA polymerases “check their work,” fixing the majority of mispaired bases in a process called proofreading. However, some errors may slip through. Post-replication mismatch repair happens right after new DNA has been made, and its job is to remove and replace mis-paired bases (ones that were not fixed during proofreading). Mismatch repair can also detect and correct small insertions and deletions that happen when the polymerases “slips,” losing its footing on the template

Question 22

Base excision repair

Answer 22

Base excision repair (BER) is a cellular mechanism that repairs damaged DNA throughout the cell cycle. It is primarily responsible for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs bulky helix-distorting lesions

Question 23

Nucleotide excision repair

Answer 23

Nucleotide excision repair (NER) is a DNA repair mechanism that is particularly important for removing DNA damage induced by ultraviolet light (UV). This damage often results in bulky DNA adducts, which are mostly thymine dimers and 6,4-photoproducts

In NER, the damaged base along with a short stretch of the surrounding healthy strand is removed, and then the gap is refilled with correct nucleotides. This process is often referred to as a ‘cut and patch’ mechanism

Question 24

Exonuclease

Answer 24

Exonucleases are enzymes that catalyze the removal of nucleotides in either the 5 to 3 or 3 to 5 direction from the ends of a single-stranded and/or double-stranded DNA

Exonucleases are enzymes that work by cleaving nucleotides one at a time from the end (exo) of a polynucleotide chain. A hydrolyzing reaction that breaks phosphodiester bonds at either the 3′ or the 5′ end occurs. Its close relative is the endonuclease, which cleaves phosphodiester bonds in the middle (endo) of a polynucleotide chain

Question 25

Mutagen

Answer 25

In genetics, a mutagen is a physical or chemical agent that permanently changes genetic material, usually DNA, in an organism and thus increases the frequency of mutations above the natural background level. As many mutations can cause cancer in animals, such mutagens can therefore be carcinogens, although not all necessarily are

ex. Tobacco, ultraviolet radiation

Question 26

Endonuclease

Answer 26

Endonucleases are enzymes that cleave the phosphodiester bond within a polynucleotide chain, such as DNA or RNA. They can break the bond from the middle of a chain. These enzymes can be either specific or non-specific to the sequences being cleaved. The endonucleases that are specific to a particular sequence are termed restriction endonucleases

Question 27

Thymine dimer

Answer 27

A thymine dimer is a molecular lesion that forms when two adjacent thymine bases in DNA bind together due to photochemical reactions, commonly associated with direct DNA damage. This process is often triggered by ultraviolet light (UV), particularly UVC, which induces the formation of covalent linkages between consecutive bases along the nucleotide chain in the vicinity of their carbon–carbon double bonds

Question 28

Cancer: Benign/malignant

Answer 28

A tumor is an abnormal mass or growth of tissue that serves no specific purpose. It can develop when cells grow and divide too quickly. Tumors can be located anywhere in the body. They grow and behave differently depending on whether they are benign (noncancerous) or malignant (cancerous)

Benign Tumors A benign tumor is made up of cells that don’t threaten to invade other tissues. The tumor cells are contained within the tumor and aren’t abnormal or very different from surrounding cells. Usually, benign types of tumors are harmless unless they are pressing on nearby tissues, nerves, or blood vessels, taking up space in the brain, causing damage, or causing excess hormone production

Question 29

Cancer: Checkpoints proteins/ p53

Answer 29

The p53 protein, also known as tumor protein p53, is a transcription factor that plays a critical role in preserving genomic integrity. It is often referred to as the “guardian of the genome” because of its crucial function. The TP53 gene, which encodes the p53 protein, is mutated in approximately half of all human malignancies, including those of the breast, colon, lung, liver, prostate, bladder, and skin

Question 30

Cancer: Tumor suppressor genes

Answer 30

Tumor suppressor genes are normal genes that slow down cell division or tell cells to die at the right time (a process known as apoptosis or programmed cell death). When tumor suppressor genes don’t work properly, cells can grow out of control, which can lead to cancer. A tumor suppressor gene is like the brake pedal on a car

Tumor suppressor genes, or antioncogenes, tell healthy cells:

• When to slow down growth
• When to repair DNA
• When to destroy themselves (a process called apoptosis that’s used for abnormal or unneeded cells)

Question 31

Cancer: Apoptosis

Answer 31

Apoptosis, also known as programmed cell death, is a process that can lead to cancer when it doesn’t function properly. It is defined by a set of physical features that are associated with the demise of an individual cell

One purpose of apoptosis is to eliminate cells that contain potentially dangerous mutations

Question 32

Cancer: Proto-oncogenes/oncogenes

Answer 32

Proto-oncogenes are genes that normally help cells grow and divide to make new cells, or to help cells stay alive. They play an important role in normal cell growth and division, and are particularly vital for the growth and development of the fetus during pregnancy. These genes function as a blueprint that codes for proteins that trigger cell growth

However, when a proto-oncogene mutates (changes) or there are too many copies of it, it can become turned on (activated) when it is not supposed to be, at which point it’s now called an oncogene

Question 33

Cancer: Mutagen

Answer 33

In genetics, a mutagen is a physical or chemical agent that permanently changes genetic material, usually DNA, in an organism and thus increases the frequency of mutations above the natural background level. As many mutations can cause cancer in animals, such mutagens can therefore be carcinogens, although not all necessarily are

Examples of mutagens include tobacco products, radioactive substances, x-rays, ultraviolet radiation, and a wide variety of chemicals

Question 34

Cancer: Metastasis

Answer 34

the process where cancer cells spread from the primary location (where the cancer began) to other regions of the body

Question 35

Cancer: Carcinogen

Answer 35

A carcinogen is any substance, agent, or organism that has the potential to cause cancer. Carcinogens may occur naturally in the environment (such as ultraviolet rays in sunlight and certain viruses) or may be generated by humans (such as automobile exhaust fumes and cigarette smoke). Most carcinogens cause cancer by producing mutations in a cell’s DNA

Carcinogens work by interacting with a cell’s DNA to produce mutations. When a carcinogen changes your DNA, it triggers a chain reaction that turns normal cells into cancerous cells. Sometimes, carcinogens do direct damage to your DNA so it stops working as it should. Other times, cells that typically repair DNA damage from carcinogens can’t take care of the issue. Left unrepaired, damaged DNA may lead to changes (mutations) in certain genes

Question 36

In Eukaryotes, a large portion of the genome does NOT code for genes. What happens when a mutation occurs there?

Answer 36

In eukaryotes, a large portion of the genome does not code for proteins. These non-coding regions contain elements that regulate gene expression, such as enhancers, transcription factor binding sites, and DNA methylation regions. Mutations in these non-coding regions can have significant effects on gene function and organism health

Here’s how:

Loss of Function: Non-coding mutations can result in reduced gene expression. This happens when the mutation affects a regulatory element in a way that it can no longer perform its function, leading to decreased production of the associated protein

Gain of Function: Non-coding mutations can also lead to gene misexpression or overexpression. This occurs when a mutation causes a gene to be turned on in the wrong place or at the wrong time, or causes an increase in the production of a protein

Structural Variations: Deletions, inversions, or duplications in non-coding regions can disturb normal chromatin folding, which can affect the 3D structure of the genome and impact gene regulation

Question 37

Which mutations would likely lead to the least amount of disturbance in a gene’s function? Which would lead to the most?

Answer 37

The least amount of disturbance in a gene’s function is typically caused by silent mutations. These mutations occur when the change in the DNA sequence does not result in a change in the amino acid sequence of the protein. This is because multiple codons (sequences of three nucleotides) can code for the same amino acid. Therefore, even if a mutation changes a codon, it might still code for the same amino acid, leading to no change in the protein’s structure.

On the other hand, frameshift mutations usually cause the most disturbance in a gene’s function. Frameshift mutations occur when one or more nucleotides are inserted or deleted from the DNA sequence. This alters the reading frame of the gene, changing the sequence of codons and, therefore, the sequence of amino acids in the protein. This can have a significant impact on the protein’s structure and function. In many cases, frameshift mutations can lead to the production of an entirely different protein, or prematurely terminate protein synthesis, which can have severe effects on an organism’s health and development.

Question 38

Are all mutations bad? Explain why or why not with examples

Answer 38

No not all are bad
ex. HIV Resistance: some people have a mutation that gives them natural resistance to the HIV virus
ex. Antibiotic Resistance in Bacteria: Constant use of antibiotics leads to the development of resistance among the targeted bacteria. These resistant bacteria do not possess the ability to reproduce as fast as those without mutation, thus slowing down the disease progression

Question 39

Discuss the differences between silent, missense, nonsense, and frameshift mutations

Answer 39

1. Silent Mutation: This type of mutation occurs when there is a change in the DNA sequence, but it does not result in a change in the amino acid sequence of the protein. This is because multiple codons (sequences of three nucleotides) can code for the same amino acid. Therefore, even if a mutation changes a codon, it might still code for the same amino acid, leading to no change in the protein’s structure
2. Missense Mutation: A missense mutation occurs when a change in the DNA sequence leads to a different codon that codes for a different amino acid. This results in a change in the amino acid sequence of the protein. Depending on where this occurs and what the change is, it can have varying effects on the protein’s function. It could have no effect, enhance the protein’s function, or render the protein faulty
3. Nonsense Mutation: Like a missense mutation, a nonsense mutation involves a change in the DNA sequence. However, in this case, the change results in a stop codon, which prematurely terminates protein synthesis. This leads to a shortened protein that may or may not function properly
4. Frameshift Mutation: Frameshift mutations occur when one or more nucleotides are inserted or deleted from the DNA sequence. This alters the reading frame of the gene, changing the sequence of codons and, therefore, the sequence of amino acids in the protein. This can have a significant impact on the protein’s structure and function

Question 40

Explain why additions and deletions cause frameshifts but substitutions do not cause

Answer 40

In DNA, the sequence of nucleotides is read in groups of three, known as codons, each of which codes for a specific amino acid.

Additions and deletions of nucleotides can cause what’s known as a frameshift mutation. This is because adding or removing nucleotides changes the way the sequence is divided into codons. For example, if you have the sequence ATGCGA and you add a T after the first nucleotide, you get TATGCGA. Now, the groups of three have shifted (from ATG CGA to TAT GCG A), changing the amino acids that are coded. This can have a major impact on the resulting protein.

On the other hand, substitutions replace one nucleotide with another but do not shift the reading frame. Using the previous example, if you replace the first G with a T, you get ATT CGA. The groups of three haven’t shifted, so only one amino acid changes. This might not affect the protein as much, especially if the new amino acid has similar properties to the old one. So, substitutions do not cause frameshifts.

Question 41

What is cancer?

Answer 41

a disease of multicellular organisms characterized by uncontrolled cell division
At least 80% of all human cancers are related to exposure to carcinogens, agents that increase the likelihood of developing cancer

Question 42

Describe at least two ways that cancer can occur via errors in oncogenes and tumor suppressor genes

Answer 42

Cancer can occur due to errors in both oncogenes and tumor suppressor genes. Here are two ways how this can happen:

Oncogenes: Oncogenes are genes that have the potential to cause cancer. In their normal state, they help regulate cell growth and division. However, when they are mutated or expressed at high levels, oncogenes can cause normal cells to become cancerous. Mutations can lead to the protein being constantly “on,” causing uncontrolled cell growth. An example of an oncogene is the HER2 gene, which is involved in cell growth and replication. Mutations and overexpression of HER2 are often seen in certain types of breast cancer.

Tumor Suppressor Genes: Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes don’t work properly, cells can grow out of control and may eventually form a tumor. For example, the TP53 gene makes the p53 protein that stops the cell cycle when there is DNA damage. If TP53 is mutated, the damaged DNA can be replicated, leading to additional mutations.

Question 43

Why is having a functional p53 gene so critical in preventing cells from becoming cancerous

Answer 43

The p53 gene is often referred to as the “guardian of the genome” because of its crucial role in preventing cells from becoming cancerous. Here’s why it’s so critical:

1. DNA Damage Checkpoint: p53 plays a key role in the cell cycle. When DNA damage is detected, p53 can halt the cell cycle and prevent the cell from dividing until the damage is repaired.
2. Apoptosis Induction: If the DNA damage is too severe and cannot be repaired, p53 can initiate a process called apoptosis, or programmed cell death. This prevents the propagation of cells with potentially harmful mutations.
3. Preventing Angiogenesis: p53 can also prevent the formation of new blood vessels (angiogenesis) that tumors need to grow and spread.
4. Regulating Metabolic Pathways: p53 helps regulate several metabolic pathways, and alterations in these pathways are often associated with cancer.

So, having a functional p53 gene is critical in maintaining the integrity of our cells and preventing the development of cancer.

Question 44

Missense mutations occur when—
a. The mutation does not alter the resulting amino acid sequence
b. The mutation causes an early stop codon
c. The addition of a nucleotide shifts the reading frame
d. The mutation causes a single amino acid to change
e. The mutation deletes a nucleotide from the gene

Answer 44

d. The mutation causes a single amino acid to change

Question 45

The random addition, deletion, or substitution of a nucleotide in the sequence of a gene is called a(n)
a. Mutation
b. Frameshift
c. Transposon
d. Allele
e. Locus

Answer 45

a. Mutation

Question 46

It is possible for a mutation to have no effect on the organism.
a. This is true
b. This is false

Answer 46

a. This is true

Question 47

Mutations occurring in somatic cells are capable of being transmitted to offspring.
a. This is true
b. This is false

Answer 47

False

Question 48

Sickle-cell anemia occurs when a point mutation results in the change of one amino acid in the code for
hemoglobin. This single change causes the hemoglobin to clump and the red blood cell to sickle. What
type of mutation is this?
a. Silent
b. Missense
c. Nonsense
d. Frameshift
e. Insertion

Answer 48

b. Missense

Question 49

This group of enzymes are involved in triggering events in the cell cycle –
a. Proteases
b. Transferases
c. Kinases
d. nucleases

Answer 49

c. kinases

Question 50

50% of cancerous cells have nonfunctioning p53 proteins. How does p53 help prevent cells from
becoming cancerous?
a. It binds growth factors
b. It checks DNA for damage
c. It induces the shift from G1 to S
d. It stops mutations from occurring
e. None of the above

Answer 50

b. It checks DNA for damage

Question 51

The Rb protein is a tumor suppressor protein that binds growth factors. Which of the following is most
likely to happen if the cell has a nonfunctional Rb protein?
a. The cell will grow faster
b. The cell will not finish the cell cycle
c. The cell will improperly replicate DNA
d. The cell will prematurely move to G0
e. The cell will undergo binary fission

Answer 51

a. The cell will grow faster

Question 52

If a cell’s proto-oncogenes are mutated and over expressed, which of the following is most likely to
happen?
a. The cell will grow faster
b. The cell will not finish the cell cycle
c. The cell will improperly replicate DNA
d. The cell will prematurely move to G0
e. The cell will undergo binary fission

Answer 52

a. the cell will grow faster