NORMAL SIGNALING PATHWAY REQUIRES Ras AND TWO PROTEINS, X AND Y signal molecule active Ras protein CYTOSOL GTP active receptor active signaling protein X tyrosine kinase The figure below shows how normal signaling works with a Ras protein acting downstream of an RTK. You examine a cell line with a constitutively active Ras protein. Signaling in this cell line can be turned off by adding a drug that -mitogen active Ras protein CYTOSOL GTP active signaling active receptor active signaling protein X protein Y tyrosine kinase | CELL DIVISON O a) prevents the ligand from binding to the RTK O b) prevents protein Y from interacting with its target O c) increases the affinity of protein Y and Ras O d) increases the activity of protein Y O e) prevents protein X from activating Ras

NORMAL SIGNALING PATHWAY REQUIRES Ras AND TWO PROTEINS, X AND Y signal molecule active Ras protein CYTOSOL GTP active receptor active signaling protein X tyrosine kinase The figure below shows how normal signaling works with a Ras protein acting downstream of an RTK. You examine a cell line with a constitutively active Ras protein. Signaling in this cell line can be turned off by adding a drug that -mitogen active Ras protein CYTOSOL GTP active signaling active receptor active signaling protein X protein Y tyrosine kinase | CELL DIVISON O a) prevents the ligand from binding to the RTK O b) prevents protein Y from interacting with its target O c) increases the affinity of protein Y and Ras O d) increases the activity of protein Y O e) prevents protein X from activating Ras

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 13RQ: A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to...

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Calcium ions (a) can act as second messengers (b) split calmodulin (c) are kept at higher concentration in the cytosol than in the extracellular fluid (d) are produced in the ER by protein kinases and protein phosphatases (e) typically terminate signaling cascades
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? EGF signaling cascades would be active for longer in the cell. EGF signaling cascades would be active for a shorter period of time in the cell. EGF signaling cascades would not occur. EGF signaling would be unaffected.
During signal transduction (a) the cell converts an extracellular signal into an intracellular signal that leads to a change in some cell process (b) a signaling molecule directly activates or represses several genes (c) each enzyme catalyzes production of one molecule of product (d) enzymes in the signal cascade remain active until the last component of the pathway alters a cellular process (e) the signal is terminated by cyclic AMP
You expressed G-protein coupled receptor T (GPCR T) and reconstituted the receptor in a synthetic phospholipid bilayer. The GPCR is activated by a ligand X, sketch the signaling pathway assuming all the necessary proteins are present.
Binding EGF to the EGF receptor causes phosphorylation of tyrosines on the cytoplasmic tail of the receptor. Which of the following best describes the mechanism by which this phosphorylation activates downstream signaling complexes? Select one A. Causes degradation of receptor by proteasome pathway B. Causes EGF receptor to be internalized so it can interact directly with downstream signaling molecules C. Tyrosine phosphorylation alters 3D structure of downstream signaling proteins causing them to change from an inactive to active conformation D. Causes release of EGF from receptor E. Alters the localization of downstream signaling partners in the cytoplasm
Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.
List two ways that GPCR signaling transduction can be turned off (go back to inactive state)
The oscillatory clock that drives somite forma-tion in vertebrates involves three essential componentsHer7 (an unstable repressor of its own synthesis), Delta (atransmembrane signaling molecule), and Notch (a trans-membrane receptor for Delta). Notch is bound by Delta onneighboring cells, activating the Notch signaling pathway,which then activates Her7 transcription. Normally, thissystem works flawlessly to create sharply defined somites(Figure Q21–2A). In the absence of Delta, however, onlythe first five somites form normally, and the rest are poorlydefined (Figure Q21–2B). If a pulse of Delta is suppliedlater, somite formation returns to normal in the regionswhere Delta was present (Figure Q21–2C). A diagram ofthe connections between the components of the clockand how they interact in adjacent cells is shown in FigureQ21–2D. In the absence of Delta, why do the cells becomeunsynchronized? What is it about the presence of Deltathat keeps adjacent cells oscillating in synchrony?
Ras uses proteins called ___________________ proteins. These proteins bridge the receptor and Ras (small monomeric G-protein) and induce Ras to release GDP and bind GTP which makes the Ras active. Active Ras can initiate a kinase cascade.
RTK: What would the following double mutations mean for the status of the signaling pathway, and the phosphorylation of MAPKK (MEK)? 1. Ligand is bound to the receptor; MAPK T120A mutation (T120 is normally phosphorylated by MAPKK) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEK 2) Ligand is not bound to the receptor; MAPKKK T132E mutation (T132 is normally phosphorylated by Ras) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEK
You isolated two mutant cells (Cell A and Cell B) which have a problem in the signal transduction pathway. Both cells show activated response to one of RTK mediated signaling without ligand, suggesting the signaling pathway has been constitutively activated by mutations. You introduced mutant Ras that blocks Ras activation step in both cells. When the mutant Ras was expressed in cell A, the signaling pathway was no longer activated. On the other hand, when the mutant Ras was expressed in cell B, the signaling pathway was still active. From these results; Q1) Which protein of the signaling pathway in Cell A might have the mutation? How does that mutation affect the function of that protein? Why do you think so? Q2) Which protein of the signaling pathway in Cell B might have the mutation? How does that mutation affect the function of that protein? Why do you think so?
Cell signaling in plant and animal cells is similar in some ways and different in others. What are some examples of this?