PCB 3023C / PCB3023C Exam 4: (Latest Update 2026 / 2027) Cell Biology | Questions & Answers | Exam study material | 100% Correct - FGCU

PCB 3023C / PCB3023C Exam 4: (Latest Update 2026 / 2027) Cell Biology | Questions & Answers | Exam study material | 100% Correct - FGCU PCB 3023 Exam 2026 / 2027 Academic Year Q: Programmed cell death occurs A. by means of an intracellular suicide program B. rarely and selectively only during animal development C. only in unhealthy or abnormal cells D. only during embryonic development A. by means of an intracellular suicide program Q: What kind of apoptosis regulator is Bcl-2? A. propoptotic B. antiapoptotic C. initiator caspase D. effector caspase B. antiapoptotic Q: Which statement about apoptosis is true? A. Cells that constitutively express Bel2 will be more prone to undergo apoptosis. B. The prodomain of procaspases contains the catalytic activity necessary for procaspase activation. C. Bax and Bak promote apoptosis by binding to procaspases in the apoptosome. D. Apoptosis is promoted by the release of cytochrome c into the cytosol from mitochondria. D. Apoptosis is promoted by the release of cytochrome c into the cytosol from mitochondria. Q: An adult hematopoietic stem cell found in the bone marrow A. will occasionally produce epidermal cells when necessary B. can produce only red blood cells C. can undergo self-renewing divisions for the lifetime of a healthy animal D. will express all the same transcription factors as those found in an unfertilized egg C. can undergo self-renewing divisions for the lifetime of a healthy animal Q: What affect would an overactive Wnt signaling pathway have on the intestinal epithelium? A. loss of stem cells for renewal of gut lining B. formation of polyps by promoting inappropriate proliferation of gut stem cells C. formation of too many absorptive cells D. formation of too few secretory cells B. formation of polyps by promoting inappropriate proliferation of gut stem cells Q: Would you consider formation of the outer layer of skin cells to be due to programmed cell death? A. yes B. no A. yes Q: How do reproductive cloning and therapeutic cloning differ? A. The DNA in the nucleus of cells produced for therapeutic cloning is genetically identical to the donor genome, whereas in cells produced for reproductive cloning it is not. B. Reproductive cloning requires a supply of fertilized donor egg cells, whereas therapeutic cloning requires unfertilized egg cells. C. Embryos are placed into foster mothers during reproductive cloning but not during therapeutic cloning. D. Therapeutic cloning requires nuclear transplantation, whereas reproductive cloning does not. A. The DNA in the nucleus of cells produced for therapeutic cloning is genetically identical to the donor genome, whereas in cells produced for reproductive cloning it is not C. Embryos are placed into foster mothers during reproductive cloning but not during therapeutic cloning. Q: Which statement about the cell cycle is false? A. Once a cell decides to enter the cell cycle, the time from start to finish is the same in all eukaryotic cells. B. An unfavorable environment can cause cells to arrest in G1. C. A cell has more DNA during G2 than it did in G1. D. The cleavage divisions that occur in an early embryo have a modified cell cycle with essentially no G1 or G2 phases. D. The cleavage divisions that occur in an early embryo have a modified cell cycle with essentially no G1 or G2 phases. Q: One approach to killing cancer cells is to induce apoptosis. Which of the following are reasonable approaches that researchers can take to induce apoptosis in cancer cells? A.activating the Bax protein B.inhibiting the Bcl2 protein C.inhibiting the p53 protein D.inhibiting the G1-cyclin-dependent kinase protein A.activating the Bax protein B.inhibiting the Bcl2 protein Q: The size of a human organ often depends on which factor?Choose one or more: A) the death of cells during its development B) the proliferation of cells during its development C) the number of chromosomes in the cells of the organ A) the death of cells during its development B) the proliferation of cells during its development Q: Which of the following statements is true?Choose one: A. Many cells die by apoptosis in many normal, adult human tissues. B. Many cells die by necrosis during normal animal development. C. Many cells die by necrosis in many normal, adult human tissues. A. Many cells die by apoptosis in many normal, adult human tissues. Q: Determine whether the following statement is true or false: Apoptosis depends on a tightly regulated proteolytic cascade. True Q: Which of the following statements is false?Choose one: A. Some death-inhibiting members of the Bcl2 family inhibit apoptosis by blocking cytochrome c release from mitochondria. B. Bax and Bak are death-promoting members of the Bcl2 family that induce the release of cytochrome c from mitochondria into the cytosol. C. The death-promoting members of the Bcl2 family include Bcl2 itself. D. Some Bcl2 family members promote apoptosis, whereas others inhibit apoptosis. C. The death-promoting members of the Bcl2 family include Bcl2 itself. Q: External signals can stimulate apoptosis by activating a set of cell-surface receptors known as what?Choose one: A) caspase receptors B) death receptors C) Bax receptors D) suicide receptors B) death receptors Q: Which of the following statements describes how mitogens operate?Choose one: A. They suppress apoptosis. B. They directly phosphorylate and activate Cdks. C. They overcome the intracellular braking mechanisms that block entry into the cell cycle. C. They overcome the intracellular braking mechanisms that block entry into the cell cycle. Q: Which of the following statements describes how growth factors stimulate animal cell enlargement?Choose one: A. They stimulate intracellular protein synthesis. B. They stimulate an influx of extracellular water into the cytosol. C. They stimulate microtubule polymerization. D. They stimulate protein degradation. A. They stimulate intracellular protein synthesis. Q: Which of the following structural changes is not typically seen in a cell that is undergoing apoptosis?Choose one: A. The nuclear envelope disassembles. B. The cell swells. C. The cell develops irregular bulges. D. The cytoskeleton collapses. B. The cell swells. Q: Mutations that prevent Bcl2 family proteins Bax and Bak from interacting with the outer mitochondrial membrane would have which effect?Choose one: A. preventing the release of cytochrome c and inhibiting apoptosis B. triggering the release of cytochrome c and promoting apoptosis C. triggering the release of cytochrome c and promoting the assembly of the apoptosome D. preventing the release of cytochrome c and promoting the assembly of the apoptosome E. preventing the release of cytochrome c and triggering the activation of procaspase-9 A. preventing the release of cytochrome c and inhibiting apoptosis Q: Investigators interested in studying the activation of apoptosis inject cytochrome c into the cytosol of two types of mammalian cells: cells that are normal and cells in which Bak and Bax have been inactivated by mutation.How would these cells be predicted to respond?Choose one: A. The normal cells will undergo apoptosis and the mutant cells will continue to grow. B. The mutant cells will undergo apoptosis and the normal cells will continue to grow. C. Neither cell type will undergo apoptosis, so both will continue to grow. D. The normal cells will undergo apoptosis and the mutant cells will die by necrosis. E. Both cell types will undergo apoptosis. E. Both cell types will undergo apoptosis. Q: In cells undergoing apoptosis, nuclear lamins are cleaved by which of the following?Choose one: A) initiator caspases B) executioner caspases C) procaspases D) nucleases B) executioner caspases Q: In response to an apoptotic stimulus, initiator caspasesChoose one: A) degrade executioner caspases. B) degrade procaspases. D) cleave a transcription factor to active gene expression. D) cleave and activate executioner caspases. D) cleave and activate executioner caspases. The surface of the villi in the small intestine is covered by a single layer of epithelial cells called enterocytes. Enterocytes absorb nutrients from the intestinal lumen as they move up the side of the villus. The enterocytes are shed from the end of the villus through apoptosis after 3 to 4 days. Consequently, new cells must be continuously supplied from the crypt and move up the villus. When a stem cell in the crypt divides, what are its immediate daughter cells? Choose one: A. a transit amplifying cell and a goblet cell B. another stem cell and a transit amplifying cell C. another stem cell and an enterocyte D. a transit amplifying cell and an enterocyte E. another stem cell and a goblet cell B. another stem cell and a transit amplifying cell Colon cancer can occur when cells in the crypt become mutated and do not migrate properly out of the crypt. Which of the following drugs could potentially block the development of colon cancer?Choose one: A. a drug that increases survival of transit amplifying cells B. a drug that leads to degradation of APC C. a drug that leads to degradation of β-catenin D. a drug that decreases differentiation of transit amplifying cells C. a drug that leads to degradation of β-catenin Determine whether the following statement is true or false: The rate of cell turnover varies in different tissue types. True Determine whether the following statement is true or false: A stem cell can only produce a single type of differentiated cell. False In the intestine, what do Wnt proteins promote?Choose one: A) apoptosis of precursor cells in each intestinal crypt B) apoptosis of the stem cells at the base of each intestinal crypt C) proliferation of the stem cells and precursor cells at the base of each intestinal crypt D) secretion of mucus at the base of each intestinal crypt C) proliferation of the stem cells and precursor cells at the base of each intestinal crypt Which of the following animal cell types, under appropriate conditions, can be kept proliferating indefinitely in culture and yet retain unrestricted developmental potential?Choose one: A. germ cells B. embryonic stem cells C. somatic cells D. proliferating precursor cells B. embryonic stem cells Which statement is true about stem cells?Choose one: A. They are totipotent, meaning that they can give rise to all cell types of the body. B. They are self-renewing and can divide for the lifetime of the organism. C. They are usually present in large numbers, especially in tissues that undergo rapid renewal. D. They are terminally differentiated. B. They are self-renewing and can divide for the lifetime of the organism. Which of these human cells undergoes the most rapid turnover?Choose one: A. red blood cells B. intestinal epithelial cells C. bone-forming cells D. nerve cells E. skin epidermal cells B. intestinal epithelial cells Hemopoietic stem cells in the bone marrow produce all of the following specialized cells EXCEPTChoose one: A) red blood cells. B) neutrophils. C) osteoclasts. D) heart muscle cells. D) heart muscle cells. Which of the following purified protein complexes would successfully drive the oocyte into M phase? Choose one: A. Purified M-Cdk/cyclin incubated with Wee1 and Cdc25 B. Purified M-Cdk/cyclin incubated with Wee1 C. Purified M-Cdk/cyclin incubated with p27 D. Purified M-Cdk alone E. Purified M-Cdk/cyclin incubated with Wee1 and p27 A. Purified M-Cdk/cyclin incubated with Wee1 and Cdc25 The Rb protein regulates the cell cycle near the end of G1. How would cell proliferation be altered by a mutation that switched all the phosphorylated serines and threonines in Rb to alanine? Choose one or more: A.Transcription of genes required for entry into S phase would decrease. B.Rb would no longer bind to the transcription regulator. C.Rb would no longer be phosphorylated. D.The cell cycle would proceed more rapidly into S phase. A.Transcription of genes required for entry into S phase would decrease. C.Rb would no longer be phosphorylated. Li-Fraumeni syndrome is a hereditary cancer syndrome characterized by high risk of developing cancer before age 30. Common cancers found in families with Li-Fraumeni: bone, breast, brain, stomach, colon, and several others. Approx 70% of families with Li-Fraumeni syndrome have inherited mutations in the p53 protein. Most often the mutations are point mutations altering single amino acids. Remember that cancer occurs when tumor cells proliferate and when their survival rate is greater than that of noncancer cells. Which of the following mutations would be consistent with the increased cancers found in individuals with Li-Fraumeni syndrome? Choose one or more: A.Mutation in p53 that increases its DNA binding activity B.Mutation in p53 so that it increases p21 gene expression C.Mutation in the phosphorylation sites on p53, so p53 is no longer phosphorylated D.Mutation in p53 so that it no longer triggers apoptosis C.Mutation in the phosphorylation sites on p53, so p53 is no longer phosphorylated D.Mutation in p53 so that it no longer triggers apoptosis Cell cycle events can be studied in the C. elegans roundworm model system as the worms have a set pattern of cell division and the early embryos are easy to observe in the microscope. The cells can also be treated with RNAi (RNA interference), which blocks gene expression of specific genes leading to a decrease in the specific protein. C. elegans oocytes are triggered to mature at the correct time by a specific M-Cdk family member. Treatment of oocytes with Wee1 RNAi triggers precocious, or early, oocyte maturation. Which of the following statements would be true in an oocyte treated with Wee1 RNAi? Choose one: A. M-Cdk would be phosphorylated on the inhibitory sites. B. M-Cdk would be found unbound from M-cyclin. C. Activated Cdc25 could block the precocious oocyte maturation. D. M-Cdk/cyclin is activated more quickly. D. M-Cdk/cyclin is activated more quickly. Which two processes together constitute the M phase of the cell cycle?Choose one: A. interphase and mitosis B. mitosis and cytokinesis C. mitosis and G0 D. S phase and metaphase E. interphase and metaphase B. mitosis and cytokinesis Which of the following processes occurs only in S phase of the cell cycle?Choose one: A. cleavage of the cytoplasm B. cell growth C. DNA replication D. organelle replication E. chromosome segregation C. DNA replication The entire period between one M phase and the subsequent M phase is called what?Choose one: A) interphase B) prophase C) G1 phase D) anaphase E) metaphase A) interphase Which of the following statements about the cell-cycle control system is not true?Choose one: A. It ensures that all DNA is replicated before M phase begins. B. It ensures that all chromosomes are attached to the mitotic spindle before the chromosomes are segregated to the two daughter cells. C. It ensures that M phase is completed before cytokinesis begins. D. It ensures that the environment is favorable for the cell to initiate DNA replication. C. It ensures that M phase is completed before cytokinesis begins. Cdk inhibitors inhibit the function of cyclin-dependent protein kinases. Different inhibitors display varying mechanisms of Cdk inhibition. Which of the following might a Cdk inhibitor block in order to block Cdk function? Choose one or more: A.substrate binding B.ATP binding C.cyclin binding D.movement of the T loop into the active site A.substrate binding B.ATP binding What is true of the basic organization and machinery of the cell cycle?Choose one: A) It is essentially the same in all living things. B) It is essentially the same in all single-celled organisms. C) It is fundamentally different in plant and animal cells. D) It is essentially the same in all eukaryotes. D) It is essentially the same in all eukaryotes. What must happen for a Cdk to be active?Choose one: A) It must be switched on by proteolysis. B) It must bind to its cyclin partner. C) It must translocate from the cytoplasm to the nucleus. D) It must increase in concentration at a specific time in the cycle. E) It must dissociate from its bound cyclin. B) It must bind to its cyclin partner. The loss of its cyclin causes a Cdk to do what?Choose one: A) phosphorylate its target proteins B) be degraded in proteasomes C) become active D) become inactive E) translocate from the cytoplasm to the nucleus D) become inactive Which of the following statements is false?Choose one: A. Activated G1-Cdks and G1/S-Cdks help drive cells through G1 into S phase. B. Activated M-Cdk triggers the onset of cytokinesis. C. Activated S-Cdk initiates DNA replication. B. Activated M-Cdk triggers the onset of cytokinesis. The cell-cycle control system uses Cdk inhibitory proteins to do what?Choose one: A) degrade cyclins B) trigger different phases of the cell cycle C) arrest the cell cycle at specific transition points D) degrade Cdks C) arrest the cell cycle at specific transition points The cell-cycle control system initiates chromosome segregation only after which of the following has occurred?Choose one: A) The cell stops growing. B) The duplicated chromosomes are correctly aligned on the mitotic spindle. C) DNA has been completely replicated and the chromosomes have decondensed. D) Cytokinesis is complete. E) M phase is complete. B) The duplicated chromosomes are correctly aligned on the mitotic spindle. These two animations illustrate how p53 binds to DNA to regulate transcription, leading to apoptosis of cells and inhibition of cancer cell growth. Several structural regions of p53 contribute to the anti-tumor function. Why is loop 2 important for p53 function?Choose one: A. Loop 2 mediates binding to other transcription factors that help regulate the anti-tumor function of p53. B. Loop 2 helps coordinate a Ca2+ ion in the Ca2+ finger. C. Loop 2 helps position a critical arginine for binding DNA. D. Loop 2 directly binds to DNA. C. Loop 2 helps position a critical arginine for binding DNA. What do cells do during G1 phase?Choose one or more: A) destroy cyclins B) separate sister chromatids C) repair DNA damage D) replicate DNA A) destroy cyclins C) repair DNA damage The signal to commence DNA replication comes from which of the following?Choose one: A) ORC B) S-Cdk C) the destruction of M-Cdk D) the destruction of Cdc6 B) S-Cdk If DNA is damaged or incompletely replicated in S phase, the inhibition of which of these molecules prevents the cell from entering M phase?Choose one: A) S-Cdk B) ORC C) p53 D) Cdc25 E) Cdc6 D) Cdc25 Which extracellular signal proteins trigger a wave of G1/S-Cdk activity?Choose one: A. death receptors B. mitogens C. growth factors D. survival factors E. death factors B. mitogens What is the mitotic spindle made of?Choose one: A) actin and myosin B) condensins C) microtubules D) cohesins C) microtubules What does the phosphorylation of Cdc25 by M-Cdk do?Choose one: A) It activates Cdc25, which in turn activates more M-Cdk. B) It activates Cdc25, which inactivates M-Cdk. C) It inactivates Cdc25, preventing further activation of M-Cdk. D) It activates Cdc25, allowing the cell to exit mitosis. E) It inactivates Cdc25, which promotes activation of more M-Cdk. A) It activates Cdc25, which in turn activates more M-Cdk. Why does the nuclear envelope break down at the start of prometaphase?Choose one: A) The growing mitotic spindle pushes through the nuclear envelope. B) The replicated chromosomes decondense. C) Nuclear lamins are unstable filaments. D) The sister chromatids separate. E) Proteins that form the nuclear pores and nuclear lamina become phosphorylated. E) Proteins that form the nuclear pores and nuclear lamina become phosphorylated. The anaphase-promoting complex or cyclosome (APC/C) triggers the onset of anaphase by doing which of the following?Choose one: A) phosphorylating the motor proteins that pull the spindle poles apart B) cleaving spindle microtubules C) triggering the destruction of the condensins that hold the duplicated chromosomes in a condensed state D) triggering the destruction of the cohesins that hold the sister chromatids together D) triggering the destruction of the cohesins that hold the sister chromatids together The chemotherapy drug paclitaxel is used to treat ovarian and breast cancers. Paclitaxel stabilizes microtubules, blocking disassembly. Paclitaxel also binds to and decreases the activity of Bcl-2. What are the two ways that paclitaxel can result in the death of cancer cells, helping to treat the cancer? Choose one or more: A.Paclitaxel inhibits cytokinesis, leading to multinucleate cells. B.Paclitaxel promotes apoptosis of the cancer cell. C.Paclitaxel disrupts the structure and integrity of the nucleus, leading to cell death. D.Paclitaxel inhibits the proper formation of the polar spindle, blocking sister chromatid separation. B.Paclitaxel promotes apoptosis of the cancer cell. D.Paclitaxel inhibits the proper formation of the polar spindle, blocking sister chromatid separation. The drug Avastin binds and inhibits VEGF. How does this drug help treat cancer?Choose one or more: A.The cancer cells are starved of oxygen. B.Angiogenesis is inhibited, blocking formation of new capillaries to the tumor. C.The drug directly kills cancer cells. D.New capillaries form and aid in delivery of chemotherapy to the tumor. A.The cancer cells are starved of oxygen. B.Angiogenesis is inhibited, blocking formation of new capillaries to the tumor. Knowledge of the driver mutations underlying cancer has led to targeted therapeutics, such as the protein kinase inhibitor imatinib (trade name Gleevec) in cases of chronic myeloid leukemia. Cancer cells often become resistant to a given drug, so researchers continue searching for new drugs that target proteins that contribute to the cancerous phenotype. One recent promising approach uses drugs that lead to ubiquitination and proteasomal degradation of the target protein. Which of the following mutated proteins are good candidates for this approach?Choose one or more: A.tumor suppressor genes B.oncogenes C.proteins with gain-of-function mutations D.proteins with loss-of-function mutations B.oncogenes C.proteins with gain-of-function mutations What is the difference between a malignant and benign tumor?Choose one: A. A malignant tumor invades and colonizes other tissues, while a benign tumor does not. B. A malignant tumor grows into a large destructive mass, whereas a benign tumor remains very small. C. A malignant tumor proliferates in defiance of normal constraints, while a benign tumor does not. D. A benign tumor grows from a single cell, whereas a malignant tumor arises from multiple cells, making it more difficult to eradicate. E. A benign tumor can be treated, while a malignant tumor cannot. A. A malignant tumor invades and colonizes other tissues, while a benign tumor does not. Cancer is fundamentally which type of disease?Choose one: A. a disease of obesity B. a genetic disease C. an infectious disease D. an environmental disease E. a human disease B. a genetic disease Which of the following is not a key behavior of cancer cells?Choose one: A. They can often proliferate indefinitely. B. They are less prone than normal cells to kill themselves by apoptosis. C. Most are genetically unstable, with a greatly increased mutation rate. D. They consume neighboring cells to fuel their excessive proliferation. E. They are abnormally invasive. D. They consume neighboring cells to fuel their excessive proliferation. Which of the following can give rise to cancer-promoting mutations?Choose one or more: A.exposure to excess sunlight B.DNA replication errors C.exposure to ionizing radiation D.inhalation of tobacco smoke A.exposure to excess sunlight B.DNA replication errors C.exposure to ionizing radiation D.inhalation of tobacco smoke Which cancer-causing gene can be activated by a single mutation in only one allele?Choose one: A. proto-oncogene B. tumor suppressor gene C. DNA repair gene A. proto-oncogene Which class of cancer-critical gene must be inactivated to promote the development of cancer?Choose one: A. oncogene B. proto-oncogene C. tumor suppressor gene C. tumor suppressor gene Many of the genes mutated in individual tumors are involved with which of the following regulatory pathways?Choose one or more: A.pathways controlling the catabolism of lactose B.pathways regulating the cell’s response to DNA damage or stress C.pathways governing the initiation of cell division B.pathways regulating the cell’s response to DNA damage or stress C.pathways governing the initiation of cell division Some cancer cells are missing a key protein needed to repair double-strand DNA breaks. They survive by relying on alternative DNA repair mechanisms. To treat these cancers, researchers have developed drugs that do which of the following?Choose one: A) promote alternative DNA repair mechanisms in normal cells B) prevent mitotic division C) inhibit alternative DNA repair mechanisms D) inhibit genetic instability C) inhibit alternative DNA repair mechanisms Which statement is true about human cells?Choose one: A. Cancer cells tend to lack telomeres. B. Cancer cells lose the ability to produce the enzyme telomerase. C. Unlike normal cells, cancer cells can only divide a limited number of times in culture. D. In cancer cells, telomeres grow progressively shorter with each cell division. E. Cancer cells maintain their telomeres by reactivating the enzyme telomerase. E. Cancer cells maintain their telomeres by reactivating the enzyme telomerase. Which type of mutation would not be involved in the inactivation of a tumor suppressor gene?Choose one: A. silencing of the gene’s activity by epigenetic changes B. loss-of-function mutation in tumor suppressor gene C. duplication of the gene D. loss of a whole chromosome containing the tumor suppressor gene E. chromosomal deletion of a region containing the tumor suppressor gene C. duplication of the gene Which of the following is most consistent with the data contained within these karyotypes? Choose one: A. The karyotype on the left is most likely from an advanced tumor due to its significant evidence of genetic instability. B. The karyotype on the left is not likely that of human and the karyotype on the right is from a normal human male. C. The karyotype on the right is most likely from an advanced tumor due to its significant evidence of genetic instability. D. The karyotype on the right is most likely from a young tumor because it is still demonstrating genetic stability. C. The karyotype on the right is most likely from an advanced tumor due to its significant evidence of genetic instability. Based on the information that is depicted in the illustration, this tumor would most likely be considered _____ because the cells _______ expressing cadherin proteins. malignant; are not Mouse embryonic stem (ES) cells A) can only be grown in the laboratory. B) can give rise to all tissues and cell types in the body except germ cells. C) can be made in the lab from human iPS cells. D) come from the inner cell mass of early embryos. D) come from the inner cell mass of early embryos. Which of the following statements about apoptosis is true? A) Cells that constitutively express Bcl2 will be more prone to undergo apoptosis. B) The prodomain of procaspases contains the catalytic activity necessary for procaspase activation. C) Bax and Bak promote apoptosis by binding to procaspases in the apoptosome. D) Apoptosis can be promoted by the release of cytochrome c into the cytosol from mitochondria. D) Apoptosis can be promoted by the release of cytochrome c into the cytosol from mitochondria. A pluripotent cell A) can only be produced in the laboratory. B) can give rise to all the tissues and cell types in the body. C) can only give rise to stem cells. D) is terminally differentiated. B) can give rise to all the tissues and cell types in the body. Which of the following best describes an abnormal situation compared to normal cells that could reasonably lead to cancer? A) increased levels of intrinsic apoptosis in cells that are proliferating B) increased levels of extrinsic apoptosis in cells that are quiescent C) increased numbers of cells induced to differentiate D) decreased frequency of apoptosis with increased cell proliferation D) decreased frequency of apoptosis with increased cell proliferation Apoptosis differs from necrosis in that necrosis A) requires the reception of an extracellular signal. B) causes DNA to fragment. C) causes cells to swell and burst, whereas apoptotic cells shrink and condense. D) involves a caspase cascade. C) causes cells to swell and burst, whereas apoptotic cells shrink and condense. Levels of Cdk activity change during the cell cycle because A. the Cdks phosphorylate each other B. the Cdks activate the cyclins C. Cdk degradation precedes entry into the next phase of the cell cycle D. cyclin levels change during the cycle D. cyclin levels change during the cycle You create cells with a version of Cdc6 that cannot be phosphorylated and thus cannot be degraded. What is the likely consequence of this change in Cdc6? A. Cells will enter another S phase prematurely. B. Cells will be unable to complete DNA synthesis. C. The origin recognition complex (ORC) will be unable to bind to DNA. D. Cde6 will be produced inappropriately during M phase. A. Cells will enter another S phase prematurely. The Retinoblastoma protein A. is a negative regulator of proliferation. B. is a positive regulator of proliferation. C. drives the transition from G, to S phase. D. blocks the transition from G, to M phase. A. is a negative regulator of proliferation. What would a cak (Cdk activating kinase) mutant look like? A. weel- B. cdc25- C. wild type B. cdc25- Which is a regulator of M-Cdk at the M checkpoint? А. АРС B. Rb C. S-Cdk D. Securin E. Cdc25 А. АРС A malignant tumor is more dangerous than a benign tumor because A. its cells are proliferating faster B. it causes neighboring cells to mutate C. its cells attack and phagocytose neighboring normal tissue cells D. its cells invade other tissues D. its cells invade other tissues Which of the following statements about cancer is false? A. Viruses cause some cancers. B. Cancer is a disease of enhanced cell proliferation and reduced cell death. C. A mutation in even a single cancer-critical gene is sufficient to convert a normal cell into a cancer cell. D. Some carcinogens cause cancer by changing the nucleotide sequence of DNA. C. A mutation in even a single cancer-critical gene is sufficient to convert a normal cell into a cancer cell. Q3. Which of the following genetic changes would not convert a proto-oncogene into an oncogene? A. A mutation that introduces a stop codon immediately after the codon for the initiator methionine. B. A mutation within the coding sequence that makes the protein hyperactive. C. An amplification of the proto-oncogene, causing overproduction of the normal protein. D. A mutation in the promoter of the proto-oncogene, causing the normal protein to be expressed at an abnormally high level. A. A mutation that introduces a stop codon immediately after the codon for the initiator methionine. Which of the following statements about tumor suppressor genes is false? A. Gene amplification of a tumor suppressor gene is less dangerous than gene amplification of a proto-oncogene. B. Cells with one functional copy of a tumor suppressor gene will usually proliferate faster than normal cells. C. Homozygous inactivation of a tumor suppressor gene leads to enhanced cell survival and proliferation. D. Individuals with only one functional copy of a tumor suppressor gene are more prone to cancer than individuals with two functional copies of a tumor suppressor gene. B. Cells with one functional copy of a tumor suppressor gene will usually proliferate faster than normal cells. A mutation in the epidermal growth factor receptor (EGFR) causes the receptor to send a positive signal along its intracellular signaling pathway even when the EGF ligand is not bound to it. This signal leads to abnormal cell proliferation in the absence of growth factor. On the basis of this information, would you classify the EGFR gene as a tumor suppressor gene or a proto-oncogene? A. tumor suppressor B. proto-oncogene C. neither B. proto-oncogene Which of the following descriptions is consistent with the behavior of a cell that lacks a protein required for a checkpoint mechanism that operates in G2? A) The cell would be unable to enter M phase. B) The cell would be unable to enter G2. C) The cell would enter M phase under conditions when normal cells would not. D) The cell would pass through M phase more slowly than normal cells. C) The cell would enter M phase under conditions when normal cells would not. Progression through the cell cycle requires a cyclin to bind to a Cdk because A) the cyclins are the molecules with the enzymatic activity in the complex. B) the binding of a cyclin to Cdk is required for Cdk enzymatic activity. C) cyclin binding inhibits Cdk activity until the appropriate time in the cell cycle. D) without cyclin binding, a cell-cycle checkpoint will be activated. B) the binding of a cyclin to Cdk is required for Cdk enzymatic activity. Levels of Cdk activity change during the cell cycle, in part because A)the Cdks phosphorylate each other. B) the Cdks activate the cyclins. C) Cdk degradation precedes entry into the next phase of the cell cycle. D) cyclin activity changes during the cycle. D) cyclin activity changes during the cycle. The retinoblastoma (Rb) protein blocks cells from entering the cell cycle by A) phosphorylating Cdk. B) marking cyclins for destruction by proteolysis. C) inhibiting cyclin transcription. D) activating apoptosis. C) inhibiting cyclin transcription How does S-Cdk help guarantee that replication occurs only once during each cell cycle? A) It blocks the rise of Cdc6 concentrations early in G1. B) It phosphorylates and inactivates DNA helicase. C) It phosphorylates and inactivates Cdc6. D) It promotes the assembly of a prereplicative complex. C) It phosphorylates and inactivates Cdc6. Which of the following types of cell-surface receptor activates the Ras and MAP kinase pathway necessary for cell-cycle progression and tumor growth? A) G-protein coupled receptor B) adherin junctions C) receptor tyrosine kinase receptors D) integrin receptors C) receptor tyrosine kinase receptors What must take place for tumor cells in an epithelial cell layer to spread and become invasive to other organs of the body? A) The cells must inactivate telomerase so that chromosomal integrity can be maintained. B) Some of the cells undergo additional DNA damage, leading to less glycosaminoglycan synthesis and a thinner, more easily penetrable basal lamina. C) A few of the tumor cells gain a mutation by chance, which activates a proteolytic enzyme (a protease) that degrades the basal lamina. D) The endothelial cells of blood vessels must mutate and penetrate through the basal lamina of an epithelial cell layer, which allows the tumor cells access to the circulatory system. C) A few of the tumor cells gain a mutation by chance, which activates a proteolytic enzyme (a protease) that degrades the basal lamina. APC is a tumor suppressor and acts in the Wnt signaling pathway to prevent the TCF complex from turning on Wnt-responsive genes. Mice that lack the gene encoding TCF4 do not have the ability to maintain the pool of proliferating gut stem cells needed to renew the gut lining. What do you predict will happen in mice that lack the Apc gene? A) Like the mice lacking TCF4, they will not be able to renew the gut lining. B) They will have inappropriate proliferation of gut stem cells. C) Mice lacking the Apc gene will have a hyperactive Wnt receptor even though there is no Wnt signal. D) Mice lacking the Apc gene will be like normal healthy mice, since APC is a tumor suppressor and thus not needed unless there is a tumor present. B) They will have inappropriate proliferation of gut stem cells. A malignant tumor is more dangerous than a benign tumor because A) its cells proliferate faster. B) it causes neighboring cells to mutate. C) its cells attack and phagocytose neighboring normal tissue cells. D) its cells invade other tissues D) its cells invade other tissues What part of an epithelial tissue needs to be degraded to allow tumor cells to spread to the rest of the body? A) tight junctions B) apical membrane proteins C) integrin receptors D) basal lamina D) basal lamina Apoptosis differs from necrosis in that necrosis res the reception of an extracellular signal. b. causes DNA to fragment. c. causes cells to swell and burst, whereas apoptotic cells shrink and condense. ves a caspase cascade. c. causes cells to swell and burst, whereas apoptotic cells shrink and condense. Which of the following represents a likely mechanism by which cells might delay entry into M if DNA replication were incomplete? a.S-Cdk complexes are inactivated. b. The phosphatase Cdc25, which normally targets an inhibitory phosphate on M-Cdk, is inhibited. C.APC/C ubiquitin ligase is not activated. d.A new round of DNA replication is initiated, and any stalled replication forks are repaired during the new round of DNA synthesis. b. The phosphatase Cdc25, which normally targets an inhibitory phosphate on M-Cdk, is inhibited. Induced pluripotent stem (iPS) cells be created by the expression of a set of key genes in most somatic cell types, including cells derived from adult tissues. re a supply of donor egg cells, as is the case for embryonic stem cells. differentiate into a greater variety of adult tissues than embryonic stem cells. been used to create human clones. be created by the expression of a set of key genes in most somatic cell types, including cells derived from adult tissues. Platelet-derived growth factor (PDGF) is both a mitogen and a growth factor. Which of the following outcomes is a likely result of PDGF action on cells expressing the PDGF receptor? er-programmed cell death by necrosis late cells to enter GO late cell proliferation at a wound site, helping with the healing process d. down-regulation of the expression of the gene encoding mitotic cyclin late cell proliferation at a wound site, helping with the healing process Ras is a GTP-binding protein that is often defective in cancer cells. A common mutation found in cancer cells causes Ras to behave as though it were bound to GTP all the time, which will cause cells to divide inappropriately. From this description, the normal Ras gene is a(n) suppressor. ene. -oncogene. -of-function mutation. -oncogene. What are the two kinds of endoplasmic reticulum Smooth and Rough What is rough ER abundant with? Cells with secretory functions because proteins that will be secreted out of the cell or inserted into the membrane What is the Golgi apparatus? A series of flattened membrane sacs localized near the nucleus What does the Golgi Apparatus do? Protein modification, packaging, and sorting to cellular locations What does the Golgi apparatus do? Produces secretory vesicles Where are all proteins synthesized and by what? In the cytosol; ribosomes How did the Nuclear membrane and ER form? Invaginations of the plasma membrane How did mitochondria form? From an anaerobic bacteria engulfing an aerobic bacteria How does a protein arrive at the correct membrane? Sorting signals in the amino acid sequence What happens if a protein lacks a sorting signal? It remains in the cytosol By what three mechanisms are proteins imported into an organelle? 1. A specialized nuclear pore that only allows certain proteins to enter 2. A protein translocator 3. Sorted in the ER and then translocated by a vesicle to appropriate organelle What are nuclear pore specifications? The proteins are folded and active transport is used When a protein is passed through a protein translocator is it folded or unfolded? Unfolded Describe sorting signals Amino acid sequence that tells where a protein should be localized to; 15-30 amino acids long; often removed but not always What is the sorting signal for the ER? Located at the amino terminal or internally, has three components of N terminal sequence, ER start sequence, and ER stop sequence; Full of leucineand hydrophobic What is the sorting signal for mitochondria? At the amino terminal and contains a lot of arginine What is the sorting signal for the nucleus? Located internally and contains a lot of lysine In what state do proteins enter the ER? while they are being synthesized What two types of proteins are synthesized in the ER? Soluble and membrane bound How is a protein imported into the ER? A signal recognition particle (SRP) binds to a ribosome synthesizing a mRNA sequence with a ER signal sequence; the SRP is then bound to an SRP receptor in the ER membrane; the ER signal sequence is then bound to the translocation channel; Protein is passed through the channel into the lumen and synthesized to completion; The terminal signal is cleaved only on the N terminal If a nucleus is more active, there will be a ______ number of pores Greater What determines the arrangement of the transmembrane protein in the ER lipid bilayer? ER signal start and stop sequences; the stop sequences are hydrophobic so the N terminus remains in the lumen, the hydrophobic portion is in the bilayer, and the C terminal is in the cytosol; If the start sequences is internal and hydrophobic then it will not be cleaved and be in the bilayer What are examples of nuclear pores allowing bidirectional transport? DNA synthesis Protein translocation What are nuclearporins? different proteins in the nuclear pores; extend like fibrils from the nuclear pore and contain a large number of binding sites for the nuclear transport receptor Nuclear pores lead from _______ to _________. Cytosol to lumen What is the NLS Nuclear localization signal What are nuclear transport receptors/import receptors? Bind to the prospective nuclear protein and then to the nucleoporin; Once in the cytosol, they dissociate and are recycled back into the cytosol What is the opposite of the nuclear import receptor? Nuclear export receptors that bind to the nuclear export signal and move to the cytosol; USES GTP What transport receptor uses GTP? Nuclear export receptor What state are the proteins in when they enter the mitochondria? Unfolded because they have a double membrane and the mitochondria can't have pores Proteins are sorted in the ________ to other organelles. ER What are the two main vesicular pathways? Exocytosis (in to out) and Endocytosis (out to in; pinocytosis, phagocytosis) What is budding driven by? assembly of a protein coat of Clathrin What does a coat of Clathrin do? Shape the membrane into a bud and capture molecules for onward transport What is Clathrin Forms a basket like molecular coating to shape membranes into vesicles What is the process of Clathrin? The cargo is attached to the cargo receptor to form the pit; The cargo receptor attaches to adaptin; This is recognized by clathrin to form the coated pit; Clathrin binds Dynamin and then the vesicle is pinched off; Clathrin is unconated from vesicle and the vesicle is transported What is v-snare? A singaling protein on a vesicle that attaches to the t-snare What do tethering proteins bind to? Rab on the vesicle membrane` How are proteins modified in the ER Disulfide bonds Glycosilation If resident ER membrane proteins escape, what happens? They contain a retrieval signal that has two lysines and two other amino acids at the C terminal end (KKXX) Resident ER membrane proteins contain what? signals that bind directly to COPI coats If resident ER soluble proteins escape, what happens? A short retrieval signal is located that the C terminal (KDEL) How do disulfide bonds form in the ER lumen Protein disulfide isomerase (PDI) is in the lumen but not the cytosol What is the function of glycosilation of ER proteins? Protects the proteins from degradation Where are proteins further stored and modified? The golgi apparatus How are proteins modified in the golgi? Addition or deletion of sugars Where do vesicles enter the golgi? Cis end Where do vesicles leave the golgi? Trans What are the folded membranes of the golgi called Cisternae What prevents misfolded or partially folded proteins from leaving the ER Chaperones What is an issue with the quality control mechanism? If the protein is mutated but fully functional, it can be retained in the ER and never reach the plasma membrane like in cystic fibrosis If a protein is still misfolded in the ER lumen after chaperone help, what happens? Sent to cytosol for degradation What do misfolded proteins in the ER trigger The unfolded protein response; Chaperones and ER expansions; The misfolded proteins bind to receptors and stimulate a transcription regulator that moves to the nucleus to activate transciption of genes of chaperones What are the steps of exocytosis? From ER to Golgi to Plasma membrane What are the two pathways of exocytosis? Constitutive Regulated What is regulated exocytosis A vesicle is transported by interacting with a hormone, neurotransmitter in the cytosol to move the vesicle to the plasma membrane Pinocytosis Cell drinking; molecules less than 150 nm Phagocytosis Cell eating; molecules greater than 250 nm How is an endocytotic vesicle formed Plasma membrane buds inward and pinches off and fuses with an endosome What is endocytosis A small amount of material is encased in the plasma membrane that buds inward and then forms to the endosome; the endosome takes the vesicle to the lysosome for degradation What is the control point for exocytosis Golgi apparatus What is the control point for endocytosis The endosome where macromolecules are sorted through What are the three fates of receptors? Degraded Recycled Moved to another surface by a ligand What range can signals act over long and short What are the four kinds of signals Endocrine Paracrine Neural Contact dependent What is an endocrine signal Hormonal, in the blood, extensive What is a paracrine signal Local mediators that are not in the blood What is a neuronal signal long distances, but direct What is contact dependent cell to cell contact and no signal is released What type of signaling controls nerve cell development contact dependent How do cells recognize signals? Receptors that become activated by one type of signal If a receptor only becomes activated by one type of signal, how does a cell fix this? Many different kinds of receptors Can each cell respond to the same receptor protein to signal? explain. Yes, acetylcholine can cause a muscle to contract, stimulate saliva, and decrease the rate of contraction of the heart but the target cell is different so there is different activity What is an example of a regulatory protein functioning on a tissue with both slow and fast response Acetylcholine acts on the heart muscle and the heart will contact in milliseconds but if it acts on the salivary glands the reaction is within one minute Why do rapid responses occur Because the target cell has the necessary proteins already in it Why do slow responses occur The signal makes changes in gene expression and the cell has to abide by those changes What are two types of rapid response? Cell movement Secretion metabolism What are two types of slow response? Increased Cell growth Cell division What are the two types of receptors? Cell surface receptors (hydrophilic; plasma membrane) and intracellular receptors (hydrophobic; either cytoplasm or nucleus) What are examples of hydrophilic ligands? Epidermal growth factor (EGF) Platelet derived growth factor (PDgF) Nerve growth factor (NGF) Transforming growth factor beta (TGF-beta) What is the nature of hydrophilic ligands? Proteins What is the nature of hydrophobic ligands? Steroid What is a hydrophobic ligand? Cortisol What is a ligand? A signaling molecule that binds to a receptor to change its conformation and therefore its function What is the pathway for a ligand-receptor interaction? Ligand binds to the receptor that changes conformation (Primary transduction) and tells (relays) intracellular signaling proteins (second messengers amplify) to activate (integrate) their target proteins to make processes in the cell occur (distribute) What are the 6 steps of signal transduction Synthesis of the signaling molecule Release of the signaling molecule Transport of signaling molecule Detection by target Response of target Removal of signal Cell surface receptors relay _________ signals by _______ pathways Extracellular; intracellular What amplifies a cell signal? A second messanger What does a second messenger do with phosphorylation? Activates a kinase downstream the messenger What are the four second messengers? Cyclic AMP (cAMP) Inositol triphosphate (IP3) Diacylglycerol (DAG) Calcium (Ca++) Receiving a messenger causes a molecule to either ________. Turn off or on Turning a molecule off or on does what? Stimulates or inhibits downstream activity What usually turns a protein on or off? Phosphorylation by kinase or dephosphorylation by phosphotase Other than phosphate, what molecule turns a protein on or off and what are these proteins? GTP; Trimeric G proteins and RAS What is the opposite of GTP binding? GTP hydrolysis What are the three main classes of cell surface receptors? Ion coupled receptors G-protein Coupled receptors* Enzyme coupled receptors* In G protein receptors, what is the membrane receptor like? 7 membrane spanning coupled to a G protein What is the structure of a G protein Alpha, Beta, and Gamma regions bound with GDP If GTP is bound to a G protein, is it on or off? On What are the two types of G proteins Gi (inhibitory) or Gs (stimulating) What do G proteins activate or repress? Ion channels and Membrane bound enzymes What part of the G protein is the functional subunit(s)? Alpha bound to GTP What is the process of G protein stimulating G protein subunits? A signal molecule attaches to the 7 membrane receptor and then GDP is hydrolyzed and GTP is bound to the alpha subunit. The beta and gamma subunits release. The GTP bound alpha subunit binds to the target proteins. Once the GTP hydrolyzes into GDP, the target protein is stimulated or activated. Alpha subunit unbinds with the target protein and then binds to the beta and gamma subunits. When a G protein stimulates activated enzymes like Adenyl cyclase, what happens? ATP hydrolysis and cAMP production is stimulated What is PLC (Phospholipase C) ? Can breakdown phosphotidylinositol biphosphate (PIP2) to generate second messengers DAG and IP3 What does IP3 stimulate the release of Ca++ What are the two enzymes G proteins act on Adenyl cyclase and Phosphotidylinositol biphosphate What does cyclic AMP do? Activates enzymes and turns on genes like Protein Kinase A (PKA) which is serine and threonine kinase Can phosphorylate enzymes to turn them on immediately Can phosphorylate proteins that regulate gene expression (Note: cAMP is a second messanger) When cyclic AMP activates Protein Kinase A, what happens? Cyclic AMP binds to the two regulatory subunits and then then the inactive catalytic subunits become active and release from Protein Kinase A What is the interaction with G proteins, cAMP, and glycogen breakdown ? In the cytosol and plasma membrane, The G protein does its stuff and activates the target protein to contact adenyl cyclase; ATP hydrolyzes and turns into cyclic AMP which activates the protein Kinase A; The Kinase then phosphorylates phosphorylase kinase with ATP and then that phosphorylase kinase phosphorylates glycogen phosphorylase to cause glycogen breakdown What is the interaction between G proteins, cAMP, and Transcription? The G protein does its stuff and activates a target protein that stimulates adenyl cyclase and releases cAMP; cAMP binds to Protein Kinase A and Protein Kinase A enter the nucleus; In the nucleus, the Protein Kinase A phosphorylates a transcription regulator to transcribe necessary genes. How does Inositol trigger the rise in intracellular calcium? The G protein is activated and the target molecule is Phospholipase C; Once phospholipase C is activated, it activates the Inositol phospholipid (IP3 and DAG) which releases from the plasma membrane as Inositol triphosphate; the Inositol triphosphate travels to the ER and opens a calcium channel; The calcium flows out and along with DAG that remained on the plasma membrane, calcium and DAG bind to Protein Kinase C How does a G protein activate an ion channel? The G protein is activated by separating alpha and GTP from beta bound to gamma; the beta gamma subunits then bind to the ion channel to open it and then unbind to close it What enzyme breaks down cAMP cAMP phoshphodiesterase to AMP What is the largest class of enzyme linked receptors Tyrosine kinases Where is the catalytic activity of tyrosine kinases In the cytoplasmic domains What kinds of activity are tyrosine kinases involved in Cellular growth Proliferation Differentiation Where is the ligand binding domain on tyrosine kinases Cytoplasmic side What are the extracellular signals for protein kinases growth factors How many transmembrane segments do RTKs have and what are they? One and an alpha helix How do tyrosine kinases work Each kinase phosphorylates the other kinase's tyrosine and then activity ensues What is an RTK receptor tyrosine kinase The binding of a dimer on the tyrosine kinases causes what The kinases to dimerize and when the intracellular tails make contact they are autophosphorylated What happens when RTKs are phosphorylated? intracellular signaling proteins bind to the tails and signaling proteins are activated What part of adaptor proteins bind to RTK SH2 domain How is an RTK turned off Phosphotases What do most RTKs activate Monomeric GTPase RAS What is RAS monomeric G protein with lipid tail in the plasma membrane; It has a GTP/GDP switch What are the two states of RAS GTP bound (active) GDP bound (inactive) When does RAS change GDP for GTP? When RAS activating protein attached to phosphorylated tyrosine RTK interacts with it What does RAS activate Kinase signaling cascade (serine/Threonine kinase) or MAP What is MAP cascade Three MAP proteins (MAPKKK, MAPKK, MAPK) which then phosphorylates effector proteins that change gene expression and protein activity and it is called the serine/threonine phosphorylating cascade When RTKs activate Phospholipid inositol 3 Kinase, what happens? Lipid docking sites in the plasma membrane are created; PI3K phosphorylates inositol phospholipids in the plasma membrane which create lipid docking sites for intracellular signaling proteins and translocation of proteins from cytosol to the plasma membrane What does it mean when AKT is activated Cell survival and growth What does BAD do? Pro-apoptotic protein What is BAD's state when it is phosphorylated It is inactivated What phosphorylates BAD AKT or Protein Kinase B Release of _______ and phosphorylation of ________ inhibits apoptosis Bcl2; BAD How does a cell grow and avoid apoptosis? A cell growth factor binds to the RTK and then the RTK autophosphorylizes; The RTK then activates a PI3K which phosphorylates inotisol phospholipid to PIP3; PIP3 phosphorylates protein Kinase 1 and protein kinase 2 interact with ATK (Protein Kinase B) to activate it; once ATK is activated, it phosphorylates BAD and the cell grows What is TOR Target of rampamycin; a serine/tyrosine kinase that enhances protein synthesis and inhibits protein degradation What inactivates TOR Rampamycin What complex does ATK specifically activate TOR What is the fast track to the nucleus pathway JAK-STAT Notch receptor signaling What are STATs Signal transducers and activators of transcription What do STATs do Move into the nucleus and stimulate the transcription of genes What activate STATs? Prolactin (Milk production) Interferons (make cells resistant to virus) What is the JAK-STAT pathway An RTK binds prolactin or interferon and then binds 2 JAK that phosphorylate and attract the STAT; The STAT is activated by phosphorylation and then forms a dimer in the cytosol; The STAT moves into the nucleus and promotes transcription of prolactin or interferon gene What does Notch receptor signaling control? neural cell development How does the Notch receptor signaling pathway work? A receptor binds to the notch receptor A delta signal protein binds to the delta notch TM receptor and the binding causes the notch receptor to cleave; The cleaved end travels into the nucleus and promotes transcription What are the four ways pathways are turned off? Metabolism of the ligand Degradation of the receptor Metabolism of the second messenger Change in the phosphorylation state of the target protein What are the four stages of the cell cyle G1 S phase (DNA replication) G2 M (mitosis and cytokinesis) What is the visible sign of the M phase Condensation of chromosomes What occurs during interphase Transcription of genes, protein synthesis (tralstion) and growth in mass What is it called when cell division is excessive Cancer What allows processes to be stopped in the cell cycle if there a malfuncitions Checkpoints What is the G2 checkpoint? Checks if all DNA is replicated and all DNA is repaired from the S phase (DNA replication) What is the G1 checkpoint? Confirms that the environment is favorable for proliferation and the DNA is intact; energy state of the cell and size of the cell What is the mitotic checkpoint? Are all the chromosomes attached to the mitotic spindle What is G0 The specialized resting state where proliferation and signals are needed for growth What is the cell cycled controlled by Cyclically activated Protein Kinases (Cdks/cyclin dependent kinases) or protein kinasaes and phosphotases What is the M phase promoting factor? Cdk What are cyclins Proteins that bind to kinases and affect their activity in the cell cycle What does a Cdk do? Phosphorylates key proteins in cell division What is Cdk activity dependent on Cyclin levels What is the main difference between cyclins and Cdk Cyclin concentration changes during the cell cycle and Cdk concentration does not because it is only present in mitosis How is a Cdk switched on and off A cyclin but also by phosphorylation and dephosphorylation; The cyclin attaches to the Cdk and then an inhibitory kinase phosphorylates the Cdk twice (Wee1) and an activating kinase phosphorylates Cdk (Cak); then an activating phosphotase (Cdc25) dephosphorylates the phosphate from Wee1 and the Cdk is activated; Cylcin attached and two phosphate What kind of feedback system does activate Cdk promote Positive feedback because it promotes the activity of the activating phosphotase enzyme Cdc25 What are cyclin concentrations regulated by? Transcription and Proteolysis; cyclin is rapidly degraded by ubiquitination once activated kinases occur What is the graph of cyclin like Gradually rises and sharply declines How is Cdk activity blocked Cdk Inhibitory proteins (CKIs) What is a CKI Cdk inhibitory protein that halts the cell cycle by blocking the formation of Cdk-cyclin complexes and helping the Cdk stay in G1 rather than move on to S What is the function of CKIs? It gives the cell more time to grow and make favorable conditions so it keeps the Cdk in the G1 phase What is an example of a CKI p27 What does a mitogen do? Promotes the production of cyclins to promote cell division What is a mitogen A cell signal protein that binds to a mitogen receptor and activates the activity and production of cyclins; The Cdk causes the phosphorylation of Rb protein which them translates the cyclin What stage is the cell cycle stuck in when there is DNA damage G1; because S is the next phase and broken DNA should not be replicated What is unprogrammed cell death? Necrosis What is programmed cell death? Apoptosis What are the three processes of apoptosis? The chromosomal DNA is fragmented and breaks up (nucleus breaks up/chromatin in small pieces) The cell shrinks and breaks up into apoptotic bodies (membrane blebbing) Phosphotidylserine moves to the outer membrane to be recognized for phagocytosis How does apoptosis know to happen/what are the two signals Intrinsic and extrinisic What are the targets of Caspases Inhibits DNAse that fragments nuclear DNA Nuclear lamins (fragments the nucleus) Cytoskeleton proteins (disrupts cytoskeleton) Membrane bleb