Biology Chapter 9, EOCQs

What is the difference between intracellular signaling and intercellular signaling?

* Intracellular signaling occurs within a cell * Intercellular signaling occurs between cells.

Cells grown in the laboratory are mixed with a dye molecule that is unable to pass through the plasma membrane. If a ligand is added to the cells, observations show that the dye enters the cells. What type of receptor did the ligand bind to on the cell surface?

An ion channel receptor opened up a pore in the membrane, which allowed the ionic dye to move into the cell.

The same second messengers are used in many different cells, but the response to second messengers is different in each cell. How is this possible?

Different cells produce different proteins, including cell-surface receptors and signaling pathway components. Therefore, they respond to different ligands, and the second messengers activate different pathways. Signal integration can also change the end result of signaling.

Pseudomonas infections are very common in hospital settings. Why would it be important for doctors to determine the bacterial load before treating an infected patient?

Doctors would need to determine if the patient is simply infected with free bacteria, or has developed a biofilm. Biofilms of Pseudomonas aeruginosa have a different pattern of gene expression than free bacteria, leading to increased virulence and resistance to many antibiotics.

If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell's behavior change?

EGF binding to EGFR initiates a signaling cascade that activates protein kinases through phosphorylation. Active Raf phosphorylates MEK, activating MEK's kinase activity. If MEK cannot be dephosphorylated, the signaling cascade downstream of MEK will continue to be active after the EGF signal is gone. Therefore, the cell will continue to proliferate, and be resistant to cell death (apoptosis).

In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP. What effect would this have on downstream cellular events?

ERK would become permanently activated, resulting in cell proliferation, migration, adhesion, and the growth of new blood vessels. Apoptosis would be inhibited.

What is a possible result of a mutation in a kinase that controls a pathway that stimulates cell growth?

If a kinase is mutated so that it is always activated, it will continuously signal through the pathway and lead to uncontrolled growth and possibly cancer. If a kinase is mutated so that it cannot function, the cell will not respond to ligand binding.

Insulin is a hormone that regulates blood sugar by binding to its receptor, insulin receptor tyrosine kinase. How does insulin's behavior differ from steroid hormone signaling, and what can you infer about its structure?

Insulin's receptor is an enzyme-linked transmembrane receptor, as can be determined from the "tyrosine kinase" in its name. This receptor is embedded in the plasma membrane, and insulin binds to its extracellular (outer) surface to initiate intracellular signaling cascades. Normally, steroid hormones cross the plasma membrane to bind with intracellular receptors. These intracellular hormone-receptor complexes then interact directly with DNA to regulate transcription. This limits steroid hormones to be small, non-polar molecules so they can cross the plasma membrane. However, since insulin does not have to cross into the cell it could be large or polar (it is a small, polar molecule).

What are the differences between internal receptors and cell-surface receptors?

Internal receptors are located inside the cell, and their ligands enter the cell to bind the receptor. The complex formed by the internal receptor and the ligand then enters the nucleus and directly affects protein production by binding to the chromosomal DNA and initiating the making of mRNA that codes for proteins. Cell surface receptors, however, are embedded in the plasma membrane, and their ligands do not enter the cell. Binding of the ligand to the cell-surface receptor initiates a cell signaling cascade and does not directly influence the making of proteins; however, it may involve the activation of intracellular proteins.

Why is signaling in multicellular organisms more complicated than signaling in single-celled organisms?

Multicellular organisms must coordinate many different events in different cell types that may be very distant from each other. Single-celled organisms are only concerned with their immediate environment and the presence of other cells in the area.

A scientist notices that a cancer cell line shows high levels of phosphorylated ERK in the absence of EGF. What are two possible explanations for the increase in phosphorylated ERK? Be specific in which proteins are involved.

Possible explanations: 1. EGFR dimer cannot separate. 2. An upstream mutation (in Ras, Raf, MEK) constitutively activates the signaling cascade. 3. ERK has a mutation that prevents it from binding to its phosphatase. 4. The cell has a mutation preventing the expression or function of the ERK-specific phosphatase.

How does the extracellular matrix control the growth of cells?

Receptors on the cell surface must be in contact with the extracellular matrix in order to receive positive signals that allow the cell to live. If the receptors are not activated by binding, the cell will undergo apoptosis. This ensures that cells are in the correct place in the body and helps to prevent invasive cell growth as occurs in metastasis in cancer.

What advantage might biofilm production confer on the S. aureus inside the catheter?

S. aureus produces a biofilm because the higher cell density in the biofilm permits the formation of a dense surface that helps protect the bacteria from antibiotics.

What would happen if the intracellular domain of a cell-surface receptor was switched with the domain from another receptor?

The binding of the ligand to the extracellular domain would activate the pathway normally activated by the receptor donating the intracellular domain.

How are the effects of paracrine signaling limited to an area near the signaling cells?

The secreted ligands are quickly removed by degradation or reabsorption into the cell so that they cannot travel far.

What characteristics make yeasts a good model for learning about signaling in humans?

Yeasts are eukaryotes and have many of the same systems that humans do; however, they are single-celled, so they are easy to grow, grow rapidly, have a short generation time, and are much simpler than humans.

Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway constriction associated with an allergic response. If a mutation in the associated G-protein's alpha subunit prevented the hydrolysis of GTP how would the allergic response change? a. More severe allergic response compared to normal G-protein signaling. b. Less severe allergic response compared to normal G-protein signaling. c. No allergic response. d. No change compared to normal G-protein signaling.

a. More severe allergic response compared to normal G protein signaling.

Endocrine signals are transmitted more slowly than paracrine signals because ___________. a. the ligands are transported through the bloodstream and travel greater distances b. the target and signaling cells are close together c. the ligands are degraded rapidly d. the ligands don't bind to carrier proteins during transport

a. the ligands are transported through the bloodstream and travel greater distances

. What is the function of a phosphatase? a. A phosphatase removes phosphorylated amino acids from proteins. b. A phosphatase removes the phosphate group from phosphorylated amino acid residues in a protein. c. A phosphatase phosphorylates serine, threonine, and tyrosine residues. d. A phosphatase degrades second messengers in the cell.

b. A phosphatase removes the phosphate group from phosphorylated amino acid residues in a protein.

A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to be stabilized by binding interactions during dimerization after ligand binding. Which hypothesis regarding the effect of this mutation on EGF signaling is most likely to be correct? a. EGF signaling cascades would be active for longer in the cell. b. EGF signaling cascades would be active for a shorter period of time in the cell. c. EGF signaling cascades would not occur. d. EGF signaling would be unaffected.

b. EGF signaling cascades would be active for a shorter period of time in the cell.

Why are ion channels necessary to transport ions into or out of a cell? a. Ions are too large to diffuse through the membrane. b. Ions are charged particles and cannot diffuse through the hydrophobic interior of the membrane. c. Ions do not need ion channels to move through the membrane. d. Ions bind to carrier proteins in the bloodstream, which must be removed before transport into the cell.

b. Ions are charged particles and cannot diffuse through the hydrophobic interior of the membrane.

How does PKC's signaling role change in response to growth factor signaling versus an immune response? a. PKC interacts directly with signaling molecules in both cascades, but only exhibits kinase activity during growth factor signaling. b. PKC interacts directly with signaling molecules in growth factor cascades, but interacts with signaling inhibitors during immune signaling. c. PKC amplifies growth factor cascades, but turns off immune cascades. d. PKC is activated during growth factor cascades, but is inactivated during immune response cascades.

b. PKC interacts directly with signaling molecules in growth factor cascades, but interacts with signaling inhibitors during immune signaling.

How does NF-κB induce gene expression? a. A small, hydrophobic ligand binds to NF-κB, activating it. b. Phosphorylation of the inhibitor Iκ-B dissociates the complex between it and NF-κB, and allows NF-κB to enter the nucleus and stimulate transcription. c. NF-κB is phosphorylated and is then free to enter the nucleus and bind DNA. d. NF-κB is a kinase that phosphorylates a transcription factor that binds DNA and promotes protein production.

b. Phosphorylation of the inhibitor Iκ-B dissociates the complex between it and NF-κB, and allows NF-κB to enter the nucleus and stimulate transcription.

What property prevents the ligands of cell-surface receptors from entering the cell? a. The molecules bind to the extracellular domain. b. The molecules are hydrophilic and cannot penetrate the hydrophobic interior of the plasma membrane. c. The molecules are attached to transport proteins that deliver them through the bloodstream to target cells. d. The ligands are able to penetrate the membrane and directly influence gene expression upon receptor binding.

b. The molecules are hydrophilic and cannot penetrate the hydrophobic interior of the plasma membrane.

Which of the following statements about quorum sensing is false? a. Autoinducer must bind to receptor to turn on transcription of genes responsible for the production of more autoinducer. b. The receptor stays in the bacterial cell, but the autoinducer diffuses out. c. Autoinducer can only act on a different cell: it cannot act on the cell in which it is made. d. Autoinducer turns on genes that enable the bacteria to form a biofilm.

c. Autoinducer can only act on a different cell: it cannot act on the cell in which it is made.

A scientist notices that when she adds a small, water-soluble molecule to a dish of cells, the cells turn off transcription of a gene. She hypothesizes that the ligand she added binds to a(n) ______ receptor. a. Intracellular b. Hormone c. Enzyme-linked d. Gated ion channel-linked

c. Enzyme-linked

HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? a. Signaling molecule binding, dimerization, and the downstream cellular response. b. Dimerization, and the downstream cellular response. c. The downstream cellular response. d. Phosphatase activity, dimerization, and the downsteam cellular response.

c. The downstream cellular response would be inhibited.

What is the effect of an inhibitor binding an enzyme? a. The enzyme is degraded. b. The enzyme is activated. c. The enzyme is inactivated. d. The complex is transported out of the cell.

c. The enzyme is inactivated.

What property enables the residues of the amino acids serine, threonine, and tyrosine to be phosphorylated? a. They are polar. b. They are non-polar. c. They contain a hydroxyl group. d. They occur more frequently in the amino acid sequence of signaling proteins.

c. They contain a hydroxyl group.

The secretion of hormones by the pituitary gland is an example of _______________. a. autocrine signaling b. paracrine signaling c. endocrine signaling d. direct signaling across gap junctions

c. endocrine signaling

Which type of molecule acts as a signaling molecule in yeasts? a. steroid b. autoinducer c. mating factor d. second messenger

c. mating factor

A scientist notices that a cancer cell line fails to die when he adds an inducer of apoptosis to his culture of cells. Which hypothesis could explain why the cells fail to die? a. The cells have a mutation that prevents the initiation of apoptosis signaling. b. The cells have lost expression of the receptor for the apoptosis-inducing ligand. c. The cells overexpress a growth factor pathway that inhibits apoptosis. d. All of the above.

d. All of the above.

A doctor is researching new ways to treat biofilms on artificial joints. Which approach would best help prevent bacterial colonization of the medical implants? a. Increase antibiotic dosing b. Create implants with rougher surfaces c. Vaccinate patients against all pathogenic bacteria d. Inhibit quorum sensing

d. Inhibit quorum sensing

Where do DAG and IP3 originate? a. They are formed by phosphorylation of cAMP. b. They are ligands expressed by signaling cells. c. They are hormones that diffuse through the plasma membrane to stimulate protein production. d. They are the cleavage products of the inositol phospholipid, PIP2.

d. They are the cleavage products of the inositol phospholipid, PIP2.

Quorum sensing is triggered to begin when ___________. a. treatment with antibiotics occurs b. bacteria release growth hormones c. bacterial protein expression is switched on d. a sufficient number of bacteria are present

d. a sufficient number of bacteria are present

Apoptosis can occur in a cell when the cell is ________________. a. damaged b. no longer needed c. infected by a virus d. all of the above

d. all of the above (damaged, no longer needed, infected by a virus)