Critical Thinking Questions

Critical Thinking Questions

21.
What is the difference between intracellular signaling and intercellular signaling?
  1. Intracellular signaling occurs between cells of two different species. Intercellular signaling occurs between two cells of the same species.
  2. Intracellular signaling occurs between two cells of same species. Intercellular signaling occurs between cells of two different species.
  3. Intracellular signaling occurs within a cell. Intercellular signaling occurs between cells.
  4. Intracellular signaling occurs between cells. Intercellular signaling occurs within cell.
22.
What are the differences between internal receptors and cell-surface receptors?
  1. Internal receptors bind to ligands that are hydrophobic and the ligand-receptor complex directly enters the nucleus, initiating transcription and translation. Cell surface receptors bind to hydrophilic ligands and initiate a signaling cascade that indirectly influences the making of a functional protein.
  2. Internal receptors bind to ligands that are hydrophilic and ligand-receptor complex directly enters the nucleus, initiating transcription and translation. Cell-surface receptors bind to hydrophobic ligands and initiate a signaling cascade that indirectly influences the making of a functional protein.
  3. Internal receptors bind to ligands that are hydrophobic and initiate the signaling cascade that indirectly influences the making of a functional protein. Cell-surface receptors bind to hydrophilic ligands and a ligand-receptor complex directly enters the nucleus, initiating transcription and translation.
  4. Internal receptors are integral membrane proteins that bind to hydrophobic ligands, initiating a signaling cascade, which indirectly influences the making of a functional protein. Cell-surface receptors bind to hydrophilic ligands and the ligand-receptor complex directly enters the nucleus, initiating transcription and translation.
23.
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, the dye is observed entering the cells. What type of receptor did the ligand bind to on the cell surface?
  1. G-protein-linked R receptor
  2. ligand-gated ion channel
  3. voltage-gated ion channel
  4. receptor tyrosine kinase
24.
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?
  1. Different cells produce the same receptor, which bind to the same ligands, but have a different response in each cell type.
  2. Cells produce variants of a particular receptor for a particular ligand through alternative splicing, resulting in different response in each cell
  3. Cells contain different genes, which produce different receptors that bind to same ligand, activating different responses in each cell.
  4. Cells produce different receptors that bind to the same ligand or the same receptor that binds to the same ligand with different signaling components, activating different responses in each cell.
25.
What would happen if the intracellular domain of a cell-surface receptor was switched with the domain from another receptor?
  1. It would activate the pathway normally triggered by the receptor that contributed the intracellular domain.
  2. It would activate the same pathway even after the intracellular domain is changed with the domain from another receptor.
  3. The receptor will be mutated and become non-functional, not activating any pathway.
  4. The receptor will become mutated and lead to continuous cell signaling, even in the absence of a ligand.
26.
Explain how a chemical that blocks the binding of EGF to the EGFR would interfere with the replication of cancerous cells that overexpress EGFR.
  1. It will activate the EGFR pathway.
  2. It will block the EGFR pathway.
  3. It will have no effect and the EGFR pathway will continue normally
  4. It will lead to overexpression of the EGFR pathway
27.
How does the extracellular matrix control the growth of cells?
  1. Contact of receptors with the extracellular matrix maintains equilibrium of the cell and provides optimal pH for the growth of the cells.
  2. Contact of the receptor with the extracellular matrix helps maintain concentration gradients across membrane, resulting in the flow of ions.
  3. The extracellular matrix provides nutrients for the cell.
  4. The extracellular matrix connects the cell to the external environment and ensures correct positioning of the cell to prevent metastasis.
28.
Give an example for each one of the following effects of a cell signal: on protein expression, cellular metabolism, and cell division.
  1. protein expression: binding of epinephrine (adrenaline) to a G-protein-linked receptor; cellular metabolism: the MAP-kinase cascade; cell division: promoted by the binding of the EGF to its receptor tyrosine kinase
  2. protein expression: the MAP-kinase cascade; cellular metabolism- binding of epinephrine (adrenaline) to a G-protein-linked receptor; cell division promoted by the binding of the EGF to its receptor tyrosine kinase
  3. protein expression: binding of the EGF to its receptor tyrosine kinase; cellular metabolism: the MAP-kinase cascade; cell division: FAS-RAS signaling.
  4. protein expression: RAS signaling; cellular metabolism: binding of the EGF to its receptor tyrosine kinase promotes an increase; cell division: binding of epinephrine (adrenaline) to a G-protein-linked receptor.
29.

The mitogen-activated protein (MAP) kinase cascade triggered by RTKs results in cell division. Create a few possible scenarios of abnormalities in the MAPK pathway leading to uncontrolled cell proliferation.

  1. gain of function mutation in RAS protein, mutation in Iκ-B, loss of function mutation in genes for MAPK kinase pathway, regulated phosphorylation cascade
  2. loss of function mutation in RAS protein and gain of function mutation in RAF protein, Iκ-B permanently bound to NF-κB, regulated phosphorylation cascade
  3. RAS protein unable to hydrolyze its bound GTP, loss of function mutation in Iκ-B, gain of function mutation in genes for MAPK kinase pathway, unregulated phosphorylation cascade
  4. unregulated phosphorylation cascade, loss of function mutation in RAS and RAF protein, mutation in genes for MAPK kinase pathway, regulated phosphorylation cascade
30.
What characteristics make yeast a good model for learning about signaling in humans?
  1. Yeasts are prokaryotes. They have a short life cycle, easy to grow, and share similarities with humans in certain regulating mechanisms.
  2. Yeasts are eukaryotes. They have a short life cycle, easy to grow, and share similarities with humans in certain regulating mechanisms.
  3. Yeasts are single-celled organisms. They have a short life cycle, easy to grow, and share similarities with humans in certain regulating mechanisms.
  4. Yeasts are single-celled organisms. They have a complex life cycle like that of humans and share similarities in regulating mechanisms.
31.
Why is signaling in multicellular organisms more complicated than signaling in single-celled organisms?
  1. Multicellular organisms coordinate between distantly located cells; single-celled organisms communicate only with nearby cells.
  2. Multicellular organisms involve receptors for signaling; single-celled organisms communicate by fusion of plasma membrane with the nearby cells.
  3. Multicellular organisms require more time for signal transduction than single-celled organisms, as they show compartmentalization.
  4. Multicellular organisms require more time for signal transduction than single-celled organisms, as they lack compartmentalization.
32.
Support the hypothesis that signaling pathways appeared early in evolution and are well-conserved using the yeast mating factor as an example.
  1. Signaling in yeast uses the RTK pathway and is evolutionarily conserved, like epinephrine signaling in humans.
  2. Signaling in yeast uses G-protein coupled receptors for signaling and is evolutionarily conserved, like epinephrine signaling in humans.
  3. Signaling in yeast uses an endocrine pathway and is evolutionarily conserved, like epinephrine signaling in humans.
  4. Mating factor in yeast uses an autocrine signaling pathway and is evolutionarily conserved, like epinephrine signaling in humans.