Flashcards in Test 3 Practice Deck (40):
True or False: Actin binds GTP while tubulin binds ATP.
False, ATP, GTP
True or False: Gelsolin is a calcium-dependent MICROTUBULE severing protein.
False, actin filament
True or False: KINESIN moves towards the plus end of microtubules while DYNEIN moves toward the minus end.
True or False: MICROTUBULES have the smallest diameter of all cytoskeletal filaments while INTERMEDIATE FILAMENTS are the largest.
False, actin filaments, microtubules
True or False: The length of the lever arm in MYSOIN motors determine the overall step length.
True or False: Cdk inhibitor proteins (CKI's) function primarily in the G1-S transition of the cell cycle.
True or False: The centrisome contains two short microtubules called CENTRIOLES.
True or False: Tight junctions form BEFORE adherens junctions.
True or False: Lamellipodia are ACTIN based-structures used for cell movement.
True or False: ER dynamics and tubule movement generally occurs on ACTIN FILAMENTS.
True or False: Thymosin and profilin are both ACTIN binding proteins.
True or False: GROWTH FACTORS promote cell division by triggering the transition through start.
True or False: Cadherin structure is strongly influenced by MAGNESIUM.
True or False: POLYGLUTAMYLATION induces curvature in microtubules.
True or False: Paracellular transport (movement between epithelial cells) is prevented primarily by ADHERENS JUNCTION.
False, tight junctions
True or False: Selectins mediate transient cell-cell interactions in CONNECTIVE TISSUES.
False, blood stream
True or False: Filamin is a MICROTUBULE binding protein that forms a gel-like state.
True or False: Kinesin binds tightly to a microtubule WITHOUT bound ATP.
True or False: NOCODOZOLE binds to ACTIN subunits and prevents their polymerization
True or False: ENDOSOMES are preferentially localized to acetylated microtubules.
Compare and contrast: Anaphase A and Anaphase B
Anaphase A: 1. Mediated by MT depolymerization of kinetochore MT at plus end. 2. Mediated by MT influx at minus end. 3. Result in chromatid separation. Anaphase B: 1. Mediated by dynein walking toward minus end with astral MTs. 2. slide force pushes the poles further apart at overlapping MTs. 3. Result in chromatid separation.
Compare and contrast: Mysoin II and Kinesin
Mysoin II: 1. Binds to actin. 2. In rigor state when ATP is not bound. 3. Works through lever arm/power stroke. 4. Works together with other myosins. Kinesin: 1. Binds to MTs. 2. Kinesin binds to ADP normally. 3. Kinesin walks head over head. 4. Kinesin works alone.
Compare and contrast: Desmosome and adherens junction
Desmosome: 1. Connect filaments of two cells together. 2. Use cadherin family proteins as adhesion molecules. 3. Connect IFs together. Adherens junction: 1. Connect filaments of two cells together. 2. Use cadherin family proteins as adhesion molecules. 3. Connect actin filaments together.
Compare and contrast: Embryonic cell cycles and adult cell cycles
Embryonic cell cycle: 1. Undergo multiple nuclear divisions before cellularization. 2. Do not rely on extracellular signals, only intracellular. 3. Much shorter interphase to rapidly increase size. Adult cell cycle: 1. Always include cytokinesis after nuclear division. 2. Rely on both intra and extracellular signals. 3. Longer interphase period.
Compare and contrast: Plasmodesmata and gap junctions
Plasmodesmata: 1. Found in plants. 2. Connect two cells together to allow small molecules and electro-currents through. 3. Close gap in response to neighboring cell damage. Gap junction: 1. Found in animals. 2. Connect two cells together to allow small molecules and electro-currents through. 3. Close gap in response to neighboring cell damage.
Compare and contrast: Condensin and cohesin
Condensin: 1. Holds together chromosomes while in the nucleus. 2. Separated by phosphorylation. 3. Phosphorylation induces chromosome condensation. Cohesin: 1. Holds together chromosomes during mitosis (outside nucleus). 2. Separated by separase.3. Separation induces chromosome splitting.
Compare and contrast: Bcl-2 and Bax
Bcl-2: 1. Anti-apoptotic protein. 2. Has 4 BH domains. 3. Inhibited by BH3 only domains. Bax: 1. Pro-apoptotic protein. 2. Has 3 BH domains. 3. Inhibited by Bcl-2.
Compare and contrast: Apoptosis and necrosis
Apoptosis: 1. Programmed cell death from inside out. 2. Either by intrinsic or extrinsic signals. 3. Does not damage neighboring cells (allows contents to be easily phagocytized). Necrosis: 1. Arises from trauma onto the cell. 2. Damages other cells from inflammation. 3. Spills all of its contents out.
Compare and contrast: Cadherin and integrin
Cadherin: 1. Adhesion protein that connects two cells through filaments. 2. Connects to itself. 3. Forms adherens junctions. Integrin: 1. Adhesion protein that connects a cell to ECM. 2. Is a dimer. 3. Forms hemidesmosomes.
The figure below shows the equilibrium distribution of actin in free subunits (monomers) and in filaments, as a function of actin concentration. Define critical concentration and indicate with an arrow where the critical concentration of actin occurs.
Critical concentration is the amount of free subunits necessary before filaments can begin to assemble without being spontaneously disassembled.
Explain why intermediate filaments have identical ends and lack polarity whereas actin filaments and microtubules have two distinct ends with a defined polarity.
Intermediate filaments are made up of several different monomeric building blocks. They form coiled-coil structures which then associate with each other to form antiparallel structures. This antiparallel structure eliminates directionality or polarity. Actin filaments are made up of a single globular monomers that attaches to one another. Microtubules use alpha-beta heterodimers to attach to one another, giving it asymmetry. Therefore, it is polar.
The drug taxol binds tightly to microtubules, stabilizing them. The drug colchicine has the opposite effect. Colchicine prevents microtubule formation. Taxol and colchicine are both toxic to growing cells and both are used as anticancer drugs. Remembering what you know about microtubule dynamics and the cell cycle, explain why both are toxic yet have opposite effects. Could the effect of these drugs be reproduced by overexpressing endogenous proteins? If so, which ones?
Taxol: Toxic because stabilizing MTs would prevent mitosis. During Anaphase, MTs must shorten to allow the chromosomes to enter the new daughter cells. Overexpression of Microtubule Associated Proteins (MAPs) would produce the same effect.
Colchicine: Toxic because mitosis requires spindle formation in order to split the chromosomes. This means that MTs must grow in order to kind the kinectochores. Overexpression of stathmin would produce the same effect because it binds to subunits and stops MT formation.
Describe, in detail, the mechanism of the near binary switch that leads to active M-CDK and the initiation of mitosis.
Inactive M-Cdk is composed of M-cyclin and Cdk1. It is held inactive by a variety of molecules. It is activated by Cdc25, which itself must first be phosphorylated by polo kinase. Once activated, M-Cdk creates a causes a near binary switch to on at the G2/M transition by phosphorylizing Cdc25 and inhibiting its own inhibitors.
Your friend comes to you in a panic. He was purifying extracts from interphase cells as well as mitotic cells. Unfortunately, the labels came off his tubes and he cannot tell which extract is from which cells. You do an experiment in which you add a small amount of each extract to fluorescent microtubules you have polymerized in vitro, and then use video microscopy to follow the behavior of individual microtubules int he reaction over time. Your results are shown in the graphs. Which extract do you think is from mitotic cells and which from interphase cells? Why?
Extract 1 is from mitotic cells. They grow larger, then suddenly begin to shorten, like what is seen at the metaphse-anaphase transition. A mitotic extract shows much fewer and shorter MTs that have an increase tendency to fragment.
Extract 2 is from interphase cells. An interphase extract yields long, relatively stable MTs with a low number of MT catastrophies.
Diagram and describe how kinetochore microtubules attach end on to the kinetochore. How is this attachment changed to generate force during mitosis?
Kinetochore MTs connect end-on to the kinetochore. This structure involves long fibrous proteins that extend from the kinetochore and terminate in a ring of proteins or collar that surround the MT some distance from the plus end. This attachment method using a sliding collar allows stable binding, but exposes the plus end of the MT for growth and shrinkage. Each spindle pole detects different levels of tension when only one kinetochore MT is attached.
Describe the structural basis of CDK activation by cyclin.
Cyclin binding alters the conformation of a particular loop of protein in the Cdk called the T-loop or activation loop. By relocating this loop away from the active site, kinase activity is promoted. However, full activation is not achieved until another kinase, called Cdk activating kinase or CAK phosphorylated a threonine residue within the T-loop.
Imagine that you can microinject cytochrome c into the cytosol of wildtype cell and of cells that lack Bax and Bak. Would you expect one, both, or neither type of cell to undergo apoptosis? Explain.
I would expect both of them to undergo apoptosis. The role of pro-apoptotic Bax and Bak is only the opening of the passage from the mitochondria into the cytosol. If you experimentally put cytochrome c into the cytosol, it will by itself find Apaf-1 and begin the intrinsic death pathway.
Embryonic tissues such as neural progenitor cells called neurospeheres form cluster in vitro. When you add EGTA you notice that the cells forming these clusters start dissociating. However, when you add calcium to the medium you can see that form clusters again. What does EGTA do and how does this effect result in tissue dissociation? Would the same effect be seen if adult tissue is used? Why?
Embryonic tissue aggregation depends on E-Cadherin, which itself is dependent on calcium to function properly. EGTA gets rid of the calcium embedded in E-Cadherin through some mechanism. When calcium is removed from Cadherin, the cadherin is no longer able to search and connect to other cadherins. Cadherin makes tissues possible by forming adherens junctions. The same would happen to adult tissue if EGTA is able to dissociate the specific cell type's cadherin.
One important role of Fas and Fas ligand is to mediate elimination of tumor cells by killer lymphocytes. In a study of 35 primary lung and colon tumors, half the tumors were found to have amplified and overexpressed a gene for a secreted protein that binds to Fas ligand. How do you suppose that overexpression of this protein might contribute to the survival of these tumor cells? Explain.
The overexpressed gene codes for a protein that is able to bind to the Fas ligand, but does not initiate the death process. Therefore, this protein reduces the amount of ligand in the extracellular fluid that could connect to Fas and actually undergo apoptosis. Within a tumor, this gene could be very dramatic because its proteins could infiltrate the entire local extracellular fluid, preventing normal cells from undergoing Fas-mediated apoptosis, thus contributing to tumor progression.