Exam 3 Chapter 17 and 18 Questions

What triggers muscle contraction?

Signals from a motor neuron tell the skeletal muscles to contract. Neurotransmitters released from the nerve terminal triggers action potential in muscle cells plasma membrane. Electrical excitement spreads into transverse tubules (membranous tubes), that extend inward from the plasma membrane around each myofibril. The signal is relayed to the sarcoplasmic reticulum. In response to the electrical excitation, Ca2+ is released from by open ion channels from the SR membrane into the cytosol. This activates a molecular switch made up of tropomyosin (rigid shaped molecule that binds in the groove of actin helix that prevent myosin heads from associating with actin filament) and troponin (protein complex that includes Ca2+ sensitive proteins associated with the end of a tropomyosin molecule). When Ca2+ concentration increases in the cytosol, Ca2+ binds to troponin and changes shape, shifting the tropomyosin molecules position, allowing myosin heads to bind, initiating muscle contraction.

Compare the structure of intermediate filaments with that of the myosin-II filaments in skeletal muscle cells. What are the major similarities? What are the major differences? How do the differences in structure relate to their function?

Similarities: - Both filaments are composed of subunits in the form of protein dimers that are held together by coiled-coil interactions. - They both have the dimer polymerize through their coiled-coil domains into filaments. Differences: - Intermediate filament dimers assemble head-to-head and create a filament with no polarity. - All myosin molecules in the same half of the mysoin filament are oriented with their heads pointing in the same direction making polarity necessary for them to be able to develop a contractile force in muscle.

What is the mechanism behind a muscle contraction?

Simultaneous shortening of all the cells sarcomeres, caused by actin filaments sliding past the myosin filaments without a change in the length of either filament. This motion is generated by myosin heads that project for the side of the myosin filaments and interact with adjacent actin filaments. When stimulated to contract, the myosin heads walk along the actin filaments in repeated cycles of attachment and detachment.

List the different types of intermediate filaments and where they are found.

- Keratin filaments found in epithelial cells. - Vimentin and vimentin-related filaments found in connective-tissue cells, muscle cells, and supporting cells of the NS. - Neurofilaments found in nerve cells. - Nuclear lamins/lamina found in nuclear envelope.

Why do you suppose it is much easier to add Tubulin to existing microtubules than to start a new microtubule from scratch? Explain how y-tubulin in the centrosome helps to overcome this hurdle.

-Tubulin is easier to be added to existing microtubules because they have more interaction sites with both end-to-end and side to side interactions. Initiating a microtubule from scratch you need a minimum number of Tubulin dimers to come together and stay together long enough for other Tubulin molecules to add to them. The Tubulin dimers need to be assembled already in order to bind the next subunits. -y-tubulin in the centrosome helps overcome this because they permanently preassemble nucleation sites (nucleating sites are referring to the assembled tubulins). The y-tubulin subunits are held tighter in side-to-side interactions allowing the alpha beta tubulin dimers to bind. This allows the ab-tubulin dimers to resemble adding to the end of an assembled microtubule.

Put the following in order from thinnest (1) to thickest (3). A) Intermediate Filaments B) Actin Filaments C) Myosin Filaments

1. Myosin 2. Intermediate 3. Actin

Describe the structure of separase.

A cystine protease enzyme that is triangular-shaped, with two lobes, and an N-Terminal tetratricopeptide repeat. They are formed in an antiparallel conformation.

Which of the following statements are correct? Explain your answers. A. Cells do not pass from G1 into M phase of the cell cycle unless there are sufficient nutrients to complete na entire cell cycle. B. Apoptosis is mediated by special intracellular protease, one of which cleaves nuclear lamins. C. Developing neurons compete for limited amounts of survival factors. D. Some vertebrate cell-cycle control proteins function when expressed in yeast cells. E.The enzymatic activity of Cdk protein is determined by both the presence of a bound cyclin and the phosphorylation state of the Cdk.

A. False. G1 doesn't go to M phase, it would be true if it said to go from G1 into S phase. B. True. Apoptosis is an active process carried out by special protease called caspases. C. True.This mechanism is thought to adjust the number of neurons to the number of specific target cells to which the neurons connect. D. True. Evolutionary conservation. E. True. Association of a Cdk protein with a cyclin is required for its activity. Dephosphorylation at specific sites on the Cdk protein is required for the cyclin-Cdk complex to be active.

One important biological effect of a large dose of ionizing radiation is to halt cell division. A. How does this occur? B. What happened if a cell has a mutation that prevents it from halting cell division after being irradiated? C. What might be the effects of such a mutation if the cell is not irradiated? D. An adult human who has reached maturity will die within a few days of receiving a radiation dose large enough to stop cell division. What does that tell you (other than that one should avoid a large dose of radiation.)

A. Radiation leads to DNA damage, and activated a regulatory mechanism that arrests the cell cycle until the DNA has been repaired. B. The cell will replicate damaged DNA and introduce mutations into the daughter cells when the cells divide. C. The cells can divide normally, but it is prone to mutations since DNA damage always occurs as a result of natural irradiation caused by cosmic rays. The mechanisms medicated by p53 is required as a safeguard against the devastating effects of accumulating DNA damage. This mechanism is not required for the natural progression of the cell cycle in undamaged cells. D. Cell division in humans is ongoing and doesn't cease upon reaching maturity. It is required for survival. Blood cells and epithelial cells in the skin or lining the gut are constantly produced by cell division to meet the body-s needs. Each day, your body produced 10^11 new red blood cells alone.

Dynamic instability causes microtubules either to grow or to shrink rapidly. Consider an individual microtubule that is in its shrinking phase. A. What must happen at the end of the microtubule in order for it to stop shrinking and to start growing again? B. How would a change in the tubulin concentration affect this switch? C. What would happen if only GDP, but no GTP, were present in the solution? D. What would happen if the solution contained an analog of GTP that cannot be hydrolyzed?

A. The microtubule is shrinking due to the loss of the GTP cap (the Tubulin subunits at its end are all in their GDP-bound form). GTP-loaded tubulin subunits from solution will still add to this end but be short-lived due to either the GTP being hydrolyzed or GTP falling off as the microtubule rim around them disassembles. if sufficient GTP-loaded subunits are added quickly enough to cover up the GDP-containing tubulin subunits at the microtubule end, a new GTP cap can form and regrowth is favored. B. The rate of addition of GTP-tubulin will be higher with higher tubulin concentrations. The frequency of the switch from shrinking microtubules to growing mode will increase with higher tubulin concentrations. The consequence being that the system is self-balancing and the more microtubules shrink, the more frequently microtubules will start to grow again. But, the more microtubules that grow, the lower the concentration of free tubulin and the rate of GTP-tubulin addition will slow down and GTP hydrolysis will catch up with new GTP-addition, GTP cap will be destroyed, and the microtubule will switch to the shrinking mode. C. With only GDP present, microtubules would continue shrinking and disappear because tubulin dimers with GDP have low affinity for each other and will not stably add to microtubules. D. If GTP was present but couldn't be hydrolyzed, microtubules would continue to grow until all free tubulin subunits are used.

Which of the following statements are correct. Explain your answers. A. Centrosomes are replicated before M phase begins. B. Two sister chromatids arise by replication of the DNA of the same chromosome and remain paired as they line up on the metaphase plate. C. Interpolar microtubules attach end-to-end and are therefore continuous from one spindle pole to the other. D. Microtubule polymerization and depolymerization and microtubule motor proteins are all required for DNA replication. E. Microtubules nucleate at the centromeres and then connect to the kinetochores, which are structures atet eh center some regions chromosomes.

A. True. Centrosomes replicate during interphase, before M phase begins. B. True. Sister chromatids separate completely only at the start of anaphase. C. False. The ends of inter polar microtubules overlap and attach to one another via proteins and motor proteins that bridge between the microtubules. D. False. Microtubules and their motor proteins don't play a role in DNA replication. E. False. The correct statement would have used centrosome instead of centromere.

Which of the following statements are correct? Explain your answers. A. Kinesin moves ER membranes along microtubules so that the network of ER tubules becomes stretched throughout the cell. B. Without actin, cells can form a functional mitotic spindle and pull their chromosomes apart but cannot divide. C. Lamellipodia and filopodia are "feelers" that a cell extends anchor points on the substratum that it will then crawl over. D. GTP is hydrolyzed by tubulin to cause the bending of flagella,. E. Cells having an intermediate-filament network that cannot be depolymerized would die. F. The plus ends of microtubules grow faster because they have a larger GTP cap. G. The transverse tubules in muscle cells are an extension of the plasma membrane, with which they are continuous; similarly, the sarcoplasmic reticulum is an extension of the ER. H. Activation of myosin movement on actin filaments is triggered by the phosphorylation of troponin in some situations and by Ca2+ binding to troponin in others.

A. True. Continual outward movement of ER is required. The absence of microtubules make the ER collapse towards the center of the cell. B. True. Actin is needed for the contractile ring causing the physical cleave between the daughter cells. The mitotic spindle that separates the chromosomes is composed of microtubules. C. True. Both extensions are associated with transmembrane proteins that protrude from the plasma membrane and enable the cell to form new anchor points on the substratum. D. False. Bending is caused ATP hydrolyzed by the dyne motor proteins that are attached tot he outer microtubules in the flagellum. E. False. Cells couldn't divide without rearranging their intermediate filaments, but some cells, like nerve cells, have stable intermediate filaments that don't depolymerize. F. False. Growth rates are independent of the size of the GTP cap. The plus and minus ends have different growth rates due to having physically distinct binding sites for incoming tubulin subunits. The rate of addition fo tubulin subunits differs at the two ends. G. True. These are both good examples of how the same membrane can have regions that are highly specialized for particular functions. H. False. Myosin movement is activated by the phosphorylation of myosin, or by calcium binding to troponin.

What do you suppose happens in mutant cells that A. cannot degrade M cyclin? B. always express high levels of p21? C. cannot phosphorylate Rb?

All three types of mutant cells would be unable to divide. A. The cells would enter mitosis but couldn't exit mitosis. B. the cells would arrest permanently in G1 because the cyclin-Cdk complexes that act in G1 would be inactivated. C. the cells would not be able to activate the transcription of genes required for cell division because the required transcription regulators would be constantly inhibited by unphosphorylated Rb.

What is the sarcoplasmic reticulum?

An adjacent sheath of interconnected flattened vesicles that surrounds each myofibril like a net stocking. Specialized muscle cell in the ER with high concentrations of Ca2+.

An antibody that binds to myosin prevents the movement of myosin molecules along actin filaments (the interaction between actin and myosin is described in Chapter 17). How do you suppose the antibody exerts this effect? What might be the result of injecting this antibody into cells (A) on the movement of chromosomes at anaphase or (B) on cytokinesis? Explain your answers.

Antibodies bind tightly to the antigen to which they were raised. When bound, an antibody can interfere with the function of the antigen by preventing it from interacting properly with other cell components. A) The movement of chromosomes at anaphase depends on microtubules and their motor proteins and does not depend on actin or myosin. Injection of an anti-myosin antibody into aa cell will therefore hav Eno effect on chromosome movement during anaphase. B) Cytokinesis depends on the assembly and contraction of. ring of actin and myosin filaments, which forms the cleavage furrow that splits the two cells. Injection of an anti-myosin antibody will therefore block cytokinesis.

Why do you think apoptosis occurs by a different mechanism from the cell death that occurs in cell necrosis? What might be the consequences if apoptosis were not achieved in so neat and orderly a fashion, whereby the cell destroys itself from within and avoids leakage of its contents into the extracellular space?

Apoptosis cant trigger a reaction that would normally associate with cell injury, due to its role in developing and adult tissues. Ex. Tissue injury would lead to the release of signal molecules that stimulate proliferation of surrounding cells so that the would heals. It also causes the release of signals that can cause a destructive inflammatory reaction. The release of intracellular content could elicit an immune response against molecules that are normally not encountered. The reactions would be self-defeating if they occur in response to the massive cell death that occurs in normal development.

Complete the following sentence accurately, explaining your reason for accepting or rejecting each of the four phrases (more than one can be correct). The role of calcium in muscle contraction is: A. to detach myosin heads from actin. B. to spread the action potential from the plasma membrane to the contractile machinery. C. to bind to troponin, cause it to move tropomyosin, and thereby expose actin filaments to myosin heads. D. to maintain the structure of the myosin filaments.

B or C will complete the sentence. Action potential directly results in the plasma membrane by the release of Ca2+ into the cytosol from the sarcoplasmic reticulum. Muscle cells are triggered to contract by the rapid rise of cytosolic Ca2+. High contraptions of Ca ions bind to troponin, causing tropomyosin to move to expose myosin-binding sites on actin filaments. A and D are wrong because Ca2+ does not effect detachment of myosin head from actin rather its the result of ATP hydrolysis. It has no role in maintaining structure of the myosin filaments.

Describe the function of myosin-II.

Binds to actin filaments to aid in muscle contraction and the contractile ring that pinches apart a dividing cell. Attaches and detaches myosin heads along the actin filament when a contraction signal is received. The heads bind and hydrolyze one molecule of ATP. This makes a conformational change and moves the tip of the head along the actin filament, creating unidirectional movement. They lose contact with the actin filaments after contraction, causing muscle relaxation. Myosin-II non-muscle cells are triggered by a rise in cytosolic Ca2+ with different mechanisms to be activated. The increase in Ca2+ cause non-muscle myosin-II to phosphorylate, altering the myosin conformation and enabling the interaction with actin. Present in smooth muscle and cardiac muscle as well. The smooth muscle can be triggered by extracellular signals including epinephrine, serotonin, prostaglandins, and more. Cardiac muscle is important for blood circulation. If there are mutations present, diseases like hypertrophic cardiomyopathy can occur.

In high highly classified research lab, Dr. Lawrence M. is charge with the task of developing aa strain of dog-sized rats to be deployed behind enemy lines. In your opinion, which of the following strategies should Dr. M. pursue to increase the size of rats. A. Block all apoptosis. B. Block p53 function. C. Overproduce growth factors, mitogens, or survival factors. Explain the likely consequences of each option.

C would be the best approach, resulting in n increase in cell number.

Why do you suppose cells have evolved a special G0 phase to exit from the cell cycle, rather than just stopping in G1, and not moving on to S phase?

Cell division control is very important. Cells must not proliferate unless it benefits the whole organism. The G0 state protects from aberrant activation of cell division because the cell-cycle control system is dismantled. If it just paused at G1, it would still contain all of the cell-cycle control system and could readily be induced to divide. The cell would have to remake the decision not to divide continuously. To re-enter the cell cycle from G0, a cell has to resynthesize all of the components that have disappeared.

A population of proliferating cells is stained with a dye that becomes fluorescent when it binds to DNA, so that the amount of fluorescence is directly proportional to the amount of DNA in each cell. To measure the amount of DNA in each cell, the cells are then passed through a flow cytometer, an instrument that measures the amount of fluorescence in individual cells. The number of cells with a given DNA content is plotted on the graph below. Indicate on the graph where you would expect to find cells that are in G1, S, G2, and mitosis. Which is the longest phase of the cell cycle in this population of cells?

Cells in peak B have twice as much DNA as those in peak A, showing that they contain replicated DNA and peak B has unreplicated DNA. Peak A contains cells in G1 and peak B has cells in G2 and mitosis. Cells in S phase have begin button finished DNA synthesis; they have various intermediate amounts of DNA and are found in the region between the two peaks. Most cells are in G1, indicating that it is the longest phase of the cell cycle.

Which of the following changes takes place when a skeletal muscle contracts? A. Z discs move farther apart. B. Actin filaments contract. C. Myosin filaments contract. D. Sarcomeres become shorter.

D. upon contraction, the Z discs move closer and neither actin nor myosin filaments contract.

Describe the structure of Intermediate filaments.

Dependent on non-covalent bonding, made up of intermediate filament proteins, with fibrous subunits that contain central elongated rod domains with distinct unstructured domains at either end (allow the formation of stable dimers by wrapping in coiled-coil configuration). Two coiled-coil dimers in opposite directions (anti-parallel) associate to form aa staggered tetramer. The tetramers assemble side by side with each other to form a rope-like intermediate filaments (think rope fibers. They all come together to form the thickness of a rope). This gives them their tensile strength. In different intermediate filaments, they all have a similar size and amino acid sequence and form similar diameters and internal structures. The terminal head and tail domains do vary in size and amino acid sequence. Structure does not depend on polarity.

Describe the function of Actin filaments.

Dependent on the ability of the filament to assemble and disassemble. Essential for cell movement, especially involving cell surface. Cells wouldn't be able to crawl or divide. They interact with action-binding proteins for different functions. Allows the adoption of different shapes. The actin monomers hydrolyze ATP to ADP after being incorporated into the filament (this reduces the strength between monomers and decreases stability of the polymer). In cell cortex, actin filaments are linked by actin-binding proteins that provide support to the plasma membrane and give mechanical strength. Actin polymerization is stopped by cytochalasin and latrunculin. Stabilized gainst depolymerization by phalloidin, freezes cell movement. Depending on associated protein: Stiff and stable structures like microvilli in epithelial cells the line the intestines. Small contractile bundles that contract and act like tiny muscles in animal cells.

Discuss the mechanisms and proteins involved in the metaphase-anaphase transition that oversees proper cell division.

During metaphase, the chromosomes are gathered at the equator of the metaphase spindles and held there, suspended under tension. The proteins that metaphase employs include motor proteins, tubulin proteins to maintain the metaphase spindle and the formation of the microtubules that hold the cells, and the kinetochore protein that is associated with the duplicated chromatids. When anaphase begins, the tension pulls the sister chromatids apart. Anaphase breaks the cohesion linkage, using the enzyme separase held by securing that is targeted by Anaphase Promoting Complex/Cyclosome , that holds the sister chromatids together. This break allows the chromosomes to be pulled towards the spindle pole that they are attached to. Tublin is lost from both ends of the kinetochore microtubules. Two motor proteins drive anaphase B, kinesin and dynein. Kinesin acts on the long, overlapping interpolar microtubules, sliding the microtubules from opposite poles past one another at the equator of the spindle and push the spindle poles apart. Dynein proteins are anchored to the plasma membrane, and move along astral microtubules to pull the poles apart.

What is the order in which the following events occur during cell division? A. anaphase B. metaphase C. prometaphase D. telophase E. mitosis F. prophase Where does cytokinesis fit in?

E is this order: FCBAD (Mitosis: prophase, prometaphase, metaphase, anaphase, telophase) Cytokinesis overlaps anaphase and telophase. Mitosis and cytokinesis are both part of M phase.

Describe the location of Intermediate filaments.

Found in the cytoplasm and nucleus of most animal cells. A network is formed throughout the cytoplasm, surrounding the nucleus, and extending out to the cell periphery, anchored at the cell-to-cell junction (desmosomes)(contact between neighboring cells in the plasma membrane). In the nucleus, they form a the nuclear lamina (meshwork) that underlies and strengthens the nuclear envelope. Abundant in muscle and epithelial cells and can occur in isolation.

Discuss the cellular mechanisms and proteins involved of the G1 checkpoint that oversees proper cell division.

G1 phase serves as a period for metabolic activity, cell growth, repair, and decides if a cell will progress further in the cell cycle to S phase or be sent to the non-proliferative state, G0. This phase uses intracellular signals that give size information and extracellular signals that reflect on environmental conditions to make this decision. During early M phase, the cell is flooded with cyclin-Cdk complexes. The S-Cdks and M-Cdks have to be disabled by the end of M phase to allow the completion of cell division and prevent initiating another round of division without time in G1. The G1 phase inactivates the S- and M-Cdks by eliminating all of the existing cyclins, blocking the synthesis or new ones, and deploying Cdk inhibitor proteins to muffle the activity of remaining cyclin-Cdk complexes. The G1 phase needs to receive mitogen signals to prevent the arrest in the G1 phase. Cyclin accumulation is required to escape G0. Mitogens are used in this to stimulate the synthesis of G1/S cyclins and other proteins involved in DNA synthesis and chromosome duplication. A buildup of these cyclins trigger a a wake of G1/S-Cdk activity and blocks G0, allowing the progression from G1 to S phase. Retinoblastoma proteins are phosphorylated to alter the conformation and release transcription regulators to active the genes required to enter S phase. If there is damage to the DNA, the cell is sent to the G0 state to prevent the replication of damaged DNA. Damaged DNA causes an increased concentration and activity of p53, a transcription regulator protein that activate the gene encoding p21, a Cdk inhibitor protein. P21 binds to the Cdks and prevents them from driving the cell into S-phase. Being sent to G0 allows for the DNA to be repaired before replication. If the DNA is too damaged, p53 initiated apoptosis. Without p53 present, unrestrained replication of damaged DNA will lead to higher rates of mutation and a higher chance of cancer.

The Golgi apparatus is thought to be partitioned into the daughter cells at cell division by a random distribution of fragments that are created at mitosis. Explain why random partitioning of chromosomes would not work.

Genetic information is distributed between multiple chromosomes. It is crucial that each daughter cell receives a copy of each chromosome when dividing. If the daughter cell receives too many or too few, the effects are deleterious or lethal. Two copies of each chromosome are produced by chromosome replication in mitosis. If the cell were to randomly distribute the chromosomes when it divided, it would be unlikely that each daughter cell would have received one copy of each chromosome. In contract, the Golgi apparatus fragments into tiny vesicles that are all alike, and by random distribution is very likely that each daughter cell will receive an approximately equal number of them.

Describe the structure of myosin.

Has two families, Myosin-I and Myosin-II. Composed of a head, neck and tail domain. Head domain is used to bind to actin and hydrolyze ATP, allowing movement along actin filaments. The neck domain links the heads and the tail. The tail helps to interact with cargo molecules and aids in mobility. They are actin-binding motor proteins. Myosin-II structure: Dimer protein with two globular ATPase heads and a single coiled-coil tail. Centrally positioned in sarcomere with action filaments extending enwrap from each end, anchored by the plus end to the Z disc. Roughly 300 myosin heads that can attach/detach about 5 times per second, enabling rapid muscle contraction. Form myosin filaments with clusters of myosin-II molecules.

Which of the following types of cells would you expect to contain a high density of intermediate filaments in their cytoplasm? Explain your answers. A. Amoeba proteus(a free-living amoeba) B. Skin epithelial cell C. Smooth muscle cell in the digestive tract D. Escherichia coli E. Nerve cell in the spinal cord F. Sperm cell G. Plant cell

High intermediate filaments in cytoplasm: -Skin epithelial cells because they need to be stiff and strong in order to maintain pressure from air, water, and rough conditions. Little amounts of intermediate filaments would lead to more susceptibility to infection and a higher chance of sustaining internal organ damages. -Smooth muscles cells in the digestive tract because they are laced around the cell to anchor the thin filaments. -Sperm cells because they need to survive the journey to the egg. -Nerve cells because they need it to make the cell strong to conduct impulses in the body. No intermediate filaments would make the nerve cells Moderate intermediate filaments in cytoplasm: -Amoeba Proteus because they are very motile. -E. coli needs them in order to keep their structure during rough external conditions No intermediate filaments in cytoplasm: -Plant cells

Describe the function of separase.

Separase works to destroy the cohesion linkage in anaphase. It is held inactive by securin during cell division until securing is degraded by APC/C and separase is released. It works by hydrolyzing Cohesin (the protein that keeps sister chromatids together).

Broadly discuss how improper rates of cell division affect human health.

Improper rates of cell division can lead to the incorrect chromosomal content, make a cell aneuploid or polyploid. If a cell is aneuploid, it will be aborted due to the absence of chromosomes. If a cell is polyploid, making a trisomy zygote. Trisomy can lead to development delays and intellectual disabilities. An example of a disorder that can result due to trisomy includes Down syndrome.

Liver cells proliferate excessively both in patients with chronic alcoholism and in patients with liver cancer. What are the differences in the mechanisms by which cell proliferation is induced in these disease?

In alcoholism, liver cells proliferate because the organ is overburdened and comes damaged by the large amounts of alcohol that has been metabolized. The need for more liver cells activates the control mechanisms that normally regulate cell proliferation. Unless badly damaged and full of scar tissue, the liver will shrink back to a normal size after the patient stops drinking excessively. In liver cancer, mutations abolish normal cell proliferation control, and the cells divide and keep on dividing an uncontrolled manner, usually fatal.

Describe the function of Intermediate filaments.

Intermediate filaments are required for a cell to withstand the mechanical stresses that occur when the cell is stretched. These filaments strengthen and protect the cell from tearing. The toughest cytoskeletal filament. Survives detergent treatment when other cytoskeletal structures don't. Ex: Found in the long length of nerve cell axons to reinforce the long an fine cell extensions. They work by distributing the effects of locally applied forces to keep cells and membranes from tearing. No role in movement, purely strength.

When cells enter mitosis, their existing array of cytoplasmic microtubules has to be rapidly broken down and replace with the mitotic spindle that forms to pull the chromosomes into the daughter cells. The enzyme katanin, named after Japanese samurai swords, is activated during the onset of mitosis, and chops microtubules into short pieces. What do you suppose is the fate of the microtubule fragments created by katanin? Explain your answer.

Katanin breaks microtubules along their length and at remote positions from their GTP caps. The fragments contain GDP-tubulin at the exposed ends and rapidly depolymerize. Katanin provides a quick means of destroying existing microtubules.

Discuss how kinases, cytoskeleton, and proteasomes are used to ensure proper rates of cell division.

Kinases are used in cell division by the employment of Cdks. Cdks are enzymes that phosphorylate specific target proteins. Cyclin becomes attached to Cdk, and the Cdk becomes activated as a kinase directing the Cdk to a specific set of target proteins appropriate for the cell cycle period controlled by cyclin. This is highly conserved. When Cdks phosphorylate, they signal that the cell is ready for the next step in the cell cycle. The cytoskeleton is important in cell division rate due to the role it plays in movement of the chromosomes during cell division. The cytoskeleton fibers are connected to different parts paired chromosomes, and are used pull them towards the poles, pulling the chromosomes apart. They are also made up of Tubulin proteins that form the spindle during cell division. Proteasome are used in ensuring proper rates of cell division due to their regulatory properties. They regulate Cdks by destroying cyclin and inactivating the Cdk. If this occurred to the M-Cdk, the inactivation allows the cell to exit mitosis.

What might be the consequence if a cell replicated damaged DNA before repairing it?

Mutations would be introduced to the two daughter cells when they divide. The mutations could increase the chances that the progeny of the affected daughter cells would eventually become cancer cells.

Describe the mechanistic involvement of myosin in cellular processes.

Myosin-II is used with actin filaments to form sarcomeres (chain like contractile units). The myosin-II muscle cells are used to contract muscles. Myosin-II non-muscle cells are activated my Ca2+ and cause a conformation change of the myosin due to phosphorylation. Myosin-I is used too enable movement across actin filaments in a cycle of binding, detachment, and rebinding. Their tails can carry cargo.

Describe the structure of Actin filaments.

Structurally dependent on polarity for the function. Thin flexible protein threads. Each filament is a twisted chain with identical globular actin monomers in the same direction along the chain (this is what makes the polarity important.). Rarely occur in isolation and generally found in cross-linked bundles. They grown by the addition of monomers (bound to a nucleoside triphosphate), fast growing. Comprised of actin protein polymers. Unstable alone but stabilize with other proteins. Can disassemble from both ends. Rearranging the actin filaments in the cortex provides the basis for a change in shape and locomotion. Can also form temporary structures (ex: dynamic protrusions) to allow the cell to crawl or the formation of a contractile ring that pinches the division of cells in the cytoplasm.

Describe how Actin filaments are used in locomotion.

The association between actin and myosin is required for movement. They work by pulling themselves across the membrane (not using flagella or cilia). Actin filament assembly is changed and pushed closer to the target by: 1) cell sending out protrusions at the front/leading edge. 2) the protrusions adhere to the surface over which the cell is crawling. 3)the rest of the cell draws itself forward by traction on these points of anchorage. Lots of free monomers = rapid filament growth with monomers added to both ends. Only some free actin= monomers are added to the plus end. The minus end hydrolyses ATP. (creating a treadmilling movement). The addition and loss is equal, allowing the movement and the remain the same size.

The shortest eukaryotic cell cycles of all—shorter even than those of many bacteria—occur in many early animal embryos. These so-called cleavage divisions take place without any significant increase in the weight of the embryo. How can this be? Which phase of the cell cycle would you expect to be most reduced?

The egg cells of many animals are big and contain stores of enough cell components to last for many cell divisions. The daughter cells that form during the first cell division after fertilization are progressively smaller in size and can be formed without a need for new protein or RNA synthesis. Whereas normally dividing cells would grow continuously in G1, G2, and S phase until they are doubled in size, there is no cell growth in these early cleavage divisions and both G1 and G2 are virtually absent. As G1 is usually longer than G2 and S phase, G1 is the most drastically reduced phase in these divisions.

What are the cellular mechanisms and proteins that contribute to sarcomere contraction?

The main protein filaments that contribute to sarcomere contractions include actin and myosin filaments. The myosin and the actin filaments are positioned in a rope like position, with the myosin filaments being centrally positioned and the actin filaments extending inward from each end anchored by the plus end to the Z disc. The minus end overlaps with the end of the myosin filaments. The muscle contraction is signaled by a sudden rise in cystolic Ca2+ rebased from the sarcoplasmic reticulum into the cytosol. A molecular switch is activated releasing troponin and tropomyosin. The troponin binds to the Ca2+, changing the shape and shifting tropomyosins position, allowing myosin heads to bind with the actin filaments and cause a contraction. Muscle contractions do not cause any shortening of the muscle cells but rather shortening of the cells sarcomeres. The myosin filaments lose all of their contact with the actin filaments once the contraction is complete, relaxing the muscle.

Describe the location of Actin filaments.

They are found in most eukaryotic cells. Fount throughout the cytoplasm and in the cell cortex (the layer beneath plasma membrane). Half of the monomers are in the cytosol, the other half are assembled into filaments. The half that is in the cytosol remain there by the use of thymosin and profilin, preventing them from joining the ends of actin filaments (regulate actin polymerization) (can be undone when needed using actin binding proteins like forming to promote polymerization).