Chapter 20 Questions - BIOL 314

Which type of junction involves a connection to the actin cytoskeleton?

adherens junctions

Proteoglycans in the extracellular matrix of animal tissues ________________.

allow cartilage to resist compression.

What are the main structures providing tensile strength in the following? A. animal connective tissue B. animal epidermis C. plant cell walls

animal connective tissue: collagen fibers, animal epidermis: intermediate filaments, plant cell walls: cellulose fibers

Induced pluripotent stem (iPS) cells ______________________.

are created by the expression of a set of key genes in cells derived from adult

Tight junctions ______________________.

are formed from claudins and occludins

Hemidesmosomes are important for ______________________.

attaching epithelial cells to the extracellular matrix.

Which of the following statements about cancer is false?

A mutation in even a single cancer-critical gene is sufficient to convert a normal cell into a cancer cell.

Which of the following genetic changes cannot convert a proto-oncogene into an oncogene?

A mutation that introduces a stop codon immediately after the codon for the initiator methionine.

Which of the following statements about tumor suppressor genes is false?

Cells with one functional copy of a tumor suppressor gene will usually proliferate faster than normal cells.

Which of the following statements about collagen is false?

Collagen synthase organizes the mature collagen molecules into ordered collagen fibrils.

__________________ join the intermediate filaments in one cell to those in the neighboring cell. __________________ anchor intermediate filaments in a cell to the extracellular matrix. __________________ involve cadherin connections between neighboring cells and are anchorage sites for actin filaments. __________________ permit the passage of small molecules from one cell to its adjacent cell. __________________ prevent the leakage of molecules between adjacent cells.

Desmosomes, hemidesmosomes, adherens junctions, gap junctions, tight junctions

Match the labeled parts of Figure Q20-20 with the phrase that best matches the part. Each part will only be used once. Figure Q20-20 basal lamina ______ apical surface _______ cell junction _______ connective tissue _______

basal lamina: B Apical surface: A cell junction: C connective tissue: D

Ras is a GTP-binding protein that is often defective in cancer cells. A common mutation found in cancer cells causes Ras to behave as though it were bound to GTP all the time, which will cause cells to divide inappropriately. From this description, the normal Ras gene is _______.

a proto-oncogene.

A metastasis is _________.

a secondary tumor in a different part of the body that arises from a cell from the primary tumor.

Adherens junctions ______________________.

can be used to bend epithelial sheets into tubes.

A pluripotent cell _________.

can give rise to all the tissues and cell types in the body.

Cells that are terminally differentiated ______________________.

can no longer undergo cell division.

An adult hemopoietic stem cell found in the bone marrow ______________________.

can undergo self-renewing divisions for the lifetime of a healthy animal.

Place the following in order of their replacement times, from shortest to longest. A. epidermal cell B. nerve cell C. bone matrix D. red blood cell E. cell lining the gut

cell lining the gut <epidermal cell < red blood cell < bone matrix <nerve cell

Which of the following molecules is not found in plants?

collagen

Mouse embryonic stem (ES) cells ______________________.

come from the inner cell mass of early embryos.

The plasmodesmata in plants are functionally most similar to which animal cell junction?

gap junction

A cell can crawl through a tissue because of the transmembrane ______________ proteins that can bind to fibronectin outside of the cell.

integrin

At desmosomes, cadherin molecules are connected to ________________.

intermediate filaments.

Indicate whether the following molecules are found in plants, animals, or both. A. intermediate filaments B. cell walls C. microtubules D. cellulose E. collagen

intermediate filaments: animals cell walls: plants microtubules: both cellulose: plants collagen: animals

A basal lamina ______________________.

is a thin layer of extracellular matrix underlying an epithelium.

A malignant tumor is more dangerous than a benign tumor because ______________________.

its cells invade other tissues.

Cadherins ______________________.

mediate cell-cell attachments through homophilic interactions.

Plants are sedentary and thus their cells have different needs from those of cells found in motile animals. For example, in plant cells, __________________ generates the turgor pressure that drives cell growth. Plants have cell walls, but cell growth is possible in the developing tissue because the __________________ cell walls are expandable. The __________________ cell walls are deposited once growth has stopped, and can be specially adapted to their function. Fibers made from __________________ (the most abundant organic macromolecule on Earth) are found in plant cell walls, and provide tensile strength. In woody tissues, the __________________ in the cell walls makes the tissue more rigid and waterproof. The deposition of the cell wall is directed by the __________________ cytoskeleton.

osmosis, primary, secondary, cellulose, lignin, microtubule

Plasmodesmata ______________________.

permit small molecules to pass from one cell to another.

When a terminally differentiated cell in an adult body dies, it can typically be replaced in the body by a stock of ________.

proliferating precursor cells.

Fibroblasts organize the collagen of the extracellular matrix by ______________.

pulling the collagen into sheets or cables after it has been secreted.

Match each name below with the best depiction of the type of epithelial sheet shown in Figure Q20-18. Each name and each picture will only be used once. Figure Q20-18 stratified ______ columnar ______ cuboidal ______ simple ______ squamous ______

stratified: C Columnar: E cuboidal: A simple: B squamous: D

An individual that arises by reproductive cloning has a nuclear genome that is identical to __________.

the adult who donated the cell for nuclear transplantation.

A major distinction between the connective tissues in an animal and other main tissue types such as epithelium, nervous tissue, or muscle is _______________.

the amount of extracellular matrix in connective tissues.

Which of the following is not an example of a connective tissue?

the layer of photoreceptors in the eye

Which type of junction contributes the most to the polarization of epithelial cells?

tight junctions

Both multicellular plants and animals have _____________________.

tissues composed of multiple different cell types.

The artificial introduction of three key ______________ into an adult cell can convert the adult cell into a cell with the properties of ES cells.

transcription factors

In 1971, Dr Judah Folkman published the "angiogenic hypothesis" suggesting that a tumor cannot grow beyond 1-2 millimeters without the development (angiogenesis) of new blood vessels that provide access to oxygen and nutrients. During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates the proliferation and migration of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF. Increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. Some evidence suggests that blocking VEGF-dependent signaling may prevent the formation of new blood vessels and lead to the death of immature blood vessels without disturbing mature blood vessels. You work for a biotechnology company that seeks to create anticancer drugs that prevent the growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. After learning about VEGF, you have a bright idea for a new mechanism of action for a potential anticancer drug. What is your idea?

1. The drug may prevent the production or secretion of VEGF by tumor cells. 2. The drug may bind free VEGF in the extracellular space, thus lowering the effective concentration of VEGF and preventing it from binding to the RTKs on epithelial cells in blood vessels (indeed, the antiangiogenesis drug Avastin® functions in this way). 3. The drug may bind to RTKs and prevent binding to VEGF or dimerization. 4. The drug may block the intracellular signaling cascade triggered when VEGF binds and activates RTKs.

Name the three key mechanisms important for maintaining the organization of cells into tissues.

1. cell communication 2. selective cell-cell adhesion 3. cell memory

Label the five different types of cell-cell junction shown in Figure Q20-26, and identify the apical and basal surfaces of the epithelium.

1: apical surface 2: tight junctions 3: adherens junction 4: desmosome junctions 5: gap junction 6: hemidesmosome junction 7: basal surface

Ras is a GTP-binding protein that is often defective in cancer cells. A signal from a growth factor through a receptor tyrosine kinase often stimulates normal cells to divide. When the receptor tyrosine kinase binds the growth factor, Ras is stimulated to bind GTP. Ras in turn activates proteins that promote cell proliferation. A common mutation in cancerous cells causes Ras to behave as though it were bound to GTP all the time. A. Why is this mutation advantageous to cancerous cells?

A Ras mutation that causes Ras to behave as though it were bound to GTP all the time is advantageous to cancer cells because Ras is then activated and turns on the activities of proteins required for cell proliferation. If the cell-proliferation proteins are always turned on, the cancer cell will be able to proliferate at an unregulated rate, outgrowing its normal neighbors. The ability to proliferate in a signal-independent fashion is one of the hallmarks of a cancer cell.

Cancer is a disease of enhanced proliferation and cell survival. DNA repair mechanisms are normally important for cell survival. When a cell senses DNA damage, the cell cycle is inhibited until the damage is fixed. Given the importance of DNA repair mechanisms, how can their failure lead to the production of cancer cells with a competitive advantage over normal cells?

A cell with a defect in its DNA repair mechanism will have an increased mutation rate, thus increasing its chances to acquire further mutations that give it (and its progeny) a competitive growth advantage.

Your friend is a pioneer in ES cell research. In her research, she uses an ES cell line that originated from an inbred strain of laboratory mice called FG426. She has just figured out methods that allow her to grow an entire liver from an ES cell and has successfully grown 10 livers. She demonstrates that the newly grown livers are functional by successfully transplanting one of the new livers into a FG426 laboratory mouse. You are particularly excited about this, because you have a sick pet mouse, Squeaky. You are very attached to Squeaky, as you found him when you were out camping in New Hampshire. Unfortunately, Squeaky has developed liver disease and will not live much longer without a liver transplant. After you see your friend on TV talking about her new method for growing mouse livers, you immediately grab your cell phone to ask her whether Squeaky could have one of the newly grown livers. Just as you are about to dial your friend, you remember something you learned in cell biology and realize that instead, you should ask your friend about possibly using therapeutic cloning for Squeaky's benefit. A. Why do you think that one of the newly grown livers may not work in Squeaky? B. Explain why therapeutic cloning would solve this problem.

A. For organ transplantation to be successful, the donor and the recipient should be as close a genetic match as possible to minimize the risk of immunological rejection. Because you found Squeaky in the fields of New Hampshire, Squeaky is likely to have genetic differences from the FG426 inbred laboratory mice. B. therapeutic cloning may help save Squeaky because it is a method for generating ES cells from Squeaky himself - cells that will be genetically identical to Squeaky. You hope that your friend will be successful when applying her methods to the Es cell line derived from Squeaky and can grow a functional liver for him.

Rb is a tumor suppressor gene; its normal function is to help restrain cell division. Loss of both copies of Rb is a causative factor in some kinds of cancer. You propose to treat these cancers by injecting the patients with a viral vector that carries a copy of the Rb gene and has the ability to infect all the cells of the body, thereby artificially driving expression of Rb in all the cells, including the cancer cells. Your colleague says "No! You'll simply kill the patient, because you will halt cell division throughout the body." A. Why would halting cell division throughout the body kill a full-grown adult person? B. Is your colleague right in thinking that forced expression of Rb in every cell will halt all cell division?

A. Many vital tissues in the adult body, including the lining of the gut, the epidermis, and the system of blood cells, require continual renewal, which is dependent on stem cells and cell division. Cessation of cell division will lead to a disappearance of these tissues, with fatal consequences. B. No, your colleague is not right to assume this. As explained in Chapter 18 (Figure 18-14), cells that express the Rb gene can proliferate: whether or not they do so depends on whether the Rb protein is phosphorylated (allowing cell division) or unphosphorylated (blocking cell division).

Match the four lettered lines in Figure Q20-13 with the appropriate numbered label. Figure Q20-13 1. integrin 2. actin 3. collagen 4. fibronectin

A: 3 B: 4 C: 1 D: 2

Which of the following statements about gap junctions is false?

Because gap junctions do not allow ions to pass through, they are not used for electrically coupling cells.

People who inherit one copy of the Rb (retinoblastoma) gene that is normal and one copy that is mutated—that is, people who are heterozygous for Rb—have a greatly increased risk of cancer. Given this information, do you agree or disagree with the following statement? Explain your answer. The Rb mutation must have a dominant effect, which means that it must result in an increase in Rb function. Thus, Rb in its mutant form must be an oncogene.

Disagree. It is true that the Rb mutation is dominant, in the sense that a person who is heterozygous (inherits one normal copy and one mutant copy of the gene) is likely to show the mutant trait (that is, will be cancer-prone). However, this does not mean that the mutation in Rb causes an increase in Rb gene function; in fact, the opposite is true—the propensity for cancer arises from a loss of Rb gene function. Therefore, Rb should be classified as a tumor suppressor gene and not as an oncogene. Most people have two functional Rb genes in each of their cells. Thus, for one of their cells to turn cancerous by losing Rb function, both copies of the gene in that cell must be inactivated or lost, a two-step process. However, in a person born lacking one copy of the Rb gene, each cell is only one step away from a complete loss of Rb function. Consequently, such a person has a high risk that at least one of the cells in the body will undergo a mutation that precipitates cancer. In this way, at the level of the whole person, the Rb loss-of-function mutation is dominant, even though at the level of the individual cell it is recessive.

Do you agree or disagree with the following statement? Explain your answer. Like many other extracellular proteins, newly synthesized collagen molecules undergo post-translational processing inside the cell to convert them into their mature form; they are then secreted and self-assemble into fibrils in the extracellular space.

Disagree. The cell secretes newly synthesized collagen molecules in an immature form as procollagen, and the peptides at the ends of the procollagen molecules then have to be cleaved off in the extracellular space before fibril assembly can occur. This process ensures that collagen fibrils will not assemble prematurely inside the cell.

How do reproductive cloning and therapeutic cloning differ?

Embryos are placed into foster mothers during reproductive cloning but not during therapeutic cloning.

Which of the following statements about integrins is false?

Integrins use adaptor proteins to interact with the microtubule cytoskeleton.

APC is a tumor suppressor and acts in the Wnt signaling pathway to prevent the TCF complex from turning on Wnt-responsive genes. Mice that lack the gene encoding TCF4 do not have the ability to maintain the pool of proliferating gut stem cells needed to renew the gut lining. What do you predict will happen in mice that lack the APC gene?

Mice lacking the APC gene will have inappropriate proliferation of gut stem cells.

Which of the following statements about cellulose is false?

Microtubules are directly attached to the outside surface of the plasma membrane to form tracks that help orient the cellulose polymers.

Drugs that block the function of oncogenic proteins hold great promise in the fight against cancer. Should cancer researchers also be attempting to design drugs that will interfere with the products of tumor suppressor genes? Explain.

Oncogenic proteins lead toward cancer, because they have excessive or unregulated activity in comparison with the corresponding normal proteins. Blocking this activity with a drug molecule that simply clogs the active site of the oncogenic protein removes the danger. For a tumor suppressor gene, the danger lies in a loss of function, and there is generally no simple way for a drug molecule to restore a protein function that has been lost. It is therefore hard to see how we could achieve any useful effect on cancer by means of drugs that interfere with tumor suppressor gene products. A drug that simply inhibited their function would be expected to promote, not cure, cancer.

Which of the following statements is false?

Proteoglycans are a major component of compact connective tissues but are relatively unimportant in watery tissues such as the jellylike substance in the interior of the eye.

Which of the following statements about animal connective tissues is true?

Proteoglycans can resist compression in the extracellular matrix.

Which of the following statements about plant cell walls is true?

The microtubule cytoskeleton directs the orientation in which cellulose is deposited in the cell wall.

A certain mutation in the receptor for epidermal growth factor (EGF) causes the mutated receptor protein to send a positive signal along the associated intracellular signaling pathway even when the EGF ligand is not bound to it. This signal leads to abnormal cell proliferation in the absence of growth factor. On the basis of this information, would you class the gene for the EGF receptor as a tumor suppressor gene or a potential oncogene? Explain your answer.

The mutation described leads toward cancerous cell behavior (excessive proliferation) by making the gene product hyperactive. The mutant gene is therefore, by definition, an oncogene. This effect is seen even if only one copy of the gene is affected; in other words, the mutation is dominant, as is typical for an oncogene. Mutations that delete an EGF receptor gene would be expected to have either no effect or an inhibiting effect on cell division. Thus, the normal EGF receptor is classed as a potential oncogene (a proto-oncogene).

A stem cell divides into two daughter cells. One of the daughter cells goes on to become a terminally differentiated cell. What is the typical fate of the other daughter cell?

The other daughter cell typically remains a stem cell

Your studies in cell biology have revealed how APC, a protein encoded by a tumor suppressor gene that is frequently inactivated in people with colorectal cancer, functions in the Wnt signaling pathway (see Figure Q20-64). This has inspired you to study Wnt signaling. You would like to design a drug to treat people with colorectal cancer. Given the pathway shown in Figure Q20-64 and the knowledge that most human colorectal tumors harbor mutations in the APC gene, name a protein from the pathway that would be a good target for an activity-blocking anticancer drug. Explain your answer.

There are two possible answers: β-catenin and TCF. Because most colorectal cancers consist of cells that lack APC, drugs that interfere directly with the Wnt signal protein, with its receptor in the cell membrane, or with the intracellular signaling protein that acts upstream of APC will not be very useful. If APC is missing, large quantities of active β-catenin will be produced even in the presence of such drugs. However, drugs that block β-catenin or TCF activity would be good candidates, provided that they do not interfere with vital functions of these proteins elsewhere in the body.

Your friend decides that the signaling pathway involving the Ras protein is a good target for drug design, because the Ras protein is often defective in cancer cells. Your friend designs a drug that will turn off the receptor tyrosine kinase by preventing it from dimerizing. Do you think that this drug will affect cells that have a defective Ras protein that acts as if it were always bound to GTP? Why or why not?

Unfortunately, a drug that blocks activation of the receptor that activates Ras will be unlikely to have a useful effect on a cell containing mutant Ras protein that behaves as though it were constantly activated. Because Ras acts downstream of the receptor, the activating mutation makes its effect felt regardless of the state of the receptor on which Ras activation would normally depend: mutant Ras that is always active is no longer dependent on the receptor for activation. Therefore, blocking the ability of the receptor to dimerize and activate Ras will probably not affect the cells containing the mutant Ras protein.

Indicate the direction in which the plant cell shown in Figure Q20-4 is most likely to grow. The black lines indicate the direction of the cellulose microfibrils around the cell. Explain your answer.

Vertically. Cellulose fibers are highly resistant to stretching, so a plant cell tends to grow, under the stimulus of turgor pressure, in a direction perpendicular to the orientation of the fibers in the cell wall.

Figure Q20-60 shows a sequence of mutations that might underlie the development of colorectal cancer. Explain why the loss of p53 is advantageous to cancerous cells.

When DNA is damaged, the protein p53 is activated and stabilized. When p53 is active, it stops the cell cycle to give the cell time to repair its damaged DNA, or, if that is not feasible, it causes the cell to commit suicide by apoptosis. Cells lacking p53 will continue to replicate their DNA, will avoid suicide, and will go through cell division even when the DNA has been damaged, producing mutant daughter cells. Repeated rounds of cell division under these circumstances perpetuate the genetic damage and allow still more mutations to occur. Some of these newly accumulated mutations will give the cell an increased ability to survive, proliferate, and metastasize, resulting in invasive cancer.