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Apoptosis is a form of cell death that occurs exclusively in multicellular organisms and is invariably triggered by external injury.
Answer: False
Explanation: Apoptosis is a highly regulated, programmed process of cell death that occurs in multicellular organisms and can also be observed in certain single-celled microorganisms. It is not exclusively triggered by external injury; internal cellular signals also initiate it.
During apoptosis, cells characteristically swell and burst, releasing their intracellular contents into the surrounding milieu.
Answer: False
Explanation: This description is characteristic of necrosis, not apoptosis. Apoptotic cells undergo shrinkage and fragmentation into membrane-bound apoptotic bodies, which prevents the release of cellular contents and subsequent inflammation.
The term 'apoptosis' is derived from Latin and signifies 'programmed cell suicide'.
Answer: False
Explanation: The term 'apoptosis' originates from Ancient Greek, meaning 'falling off,' analogous to petals falling from a flower or leaves from a tree. It describes a controlled process of cell death, not necessarily 'suicide'.
John Kerr, Alastair Currie, and Andrew Wyllie are credited with popularizing the term 'apoptosis' through a seminal article published in 1972.
Answer: True
Explanation: Indeed, the work of Kerr, Currie, and Wyllie was instrumental in distinguishing apoptosis from traumatic cell death and in establishing the term 'apoptosis' within the scientific lexicon.
During apoptosis, cells typically swell and burst, releasing their contents into surrounding tissues.
Answer: False
Explanation: This description aligns with necrosis. Apoptosis involves cellular shrinkage and fragmentation into membrane-bound apoptotic bodies, thereby preventing the release of cellular contents and minimizing inflammation.
Sydney Brenner, H. Robert Horvitz, and John Sulston received the Nobel Prize for identifying genes controlling apoptosis in fruit flies.
Answer: False
Explanation: Brenner, Horvitz, and Sulston were awarded the Nobel Prize in Physiology or Medicine in 2002 for their discoveries concerning 'genetic regulation of organ development and programmed cell death,' primarily through studies in the nematode *C. elegans*, not fruit flies.
Apoptotic cell disassembly involves the formation of membrane protrusions called apoptopodia and fragmentation into apoptotic bodies.
Answer: True
Explanation: This accurately describes the morphological changes during the dismantling phase of apoptosis, where the cell undergoes controlled fragmentation into manageable apoptotic bodies.
DNA laddering is a characteristic pattern of DNA fragmentation observed in necrosis but not in apoptosis.
Answer: False
Explanation: DNA laddering, representing the cleavage of DNA into nucleosomal fragments, is a hallmark of apoptosis, not necrosis. Necrosis typically results in random DNA degradation.
What is apoptosis primarily defined as?
Answer: A highly regulated, programmed process of cell death.
Explanation: Apoptosis is fundamentally characterized as a highly regulated and programmed sequence of events leading to cell death, distinct from uncontrolled necrotic cell death.
Which of the following is a key morphological change observed during apoptosis?
Answer: Chromatin condensation into patches against the nuclear envelope.
Explanation: Chromatin condensation (pyknosis) and fragmentation (karyorrhexis) against the nuclear envelope are characteristic morphological features of apoptosis, alongside cellular shrinkage and membrane blebbing.
How does apoptosis fundamentally differ from necrosis in terms of cellular contents?
Answer: Necrosis involves cell swelling and lysis, releasing contents, while apoptosis forms membrane-bound apoptotic bodies that prevent leakage.
Explanation: The critical distinction lies in the containment of cellular components. Necrosis leads to lysis and release, whereas apoptosis results in the formation of apoptotic bodies, which are phagocytosed without eliciting an inflammatory response.
The term 'apoptosis' was adopted into medical terminology from Ancient Greek, meaning:
Answer: Falling off
Explanation: The term 'apoptosis' is derived from the Greek words 'apo' (off) and 'ptosis' (falling), evoking the natural process of leaves or petals detaching.
Which group of scientists is primarily credited with distinguishing apoptosis from traumatic cell death and popularizing the term?
Answer: John Kerr, Alastair Currie, and Andrew Wyllie
Explanation: While Vogt and Flemming provided early descriptions, it was Kerr, Currie, and Wyllie's 1972 publication that significantly advanced the understanding and popularization of apoptosis as a distinct biological process.
What major event significantly boosted apoptosis research and linked it to diseases like cancer?
Answer: The identification of the BCL2 gene inhibiting cell death.
Explanation: The discovery that the BCL2 gene inhibits cell death was pivotal, demonstrating a molecular basis for apoptosis regulation and strongly linking its dysregulation to oncogenesis, thereby elevating apoptosis research.
The discovery of the BCL2 gene's role in inhibiting cell death significantly boosted apoptosis research, particularly its link to cancer.
Answer: True
Explanation: The identification of BCL2 as an inhibitor of apoptosis was a landmark finding, establishing a direct molecular link between apoptosis dysregulation and cancer development, thereby galvanizing research in the field.
Bax and Bak proteins prevent apoptosis by stabilizing the mitochondrial membrane.
Answer: False
Explanation: Bax and Bak proteins are pro-apoptotic members of the Bcl-2 family. They promote apoptosis by forming pores in the outer mitochondrial membrane, thereby facilitating the release of cytochrome c and other pro-apoptotic factors.
Caspases are enzymes that build cellular structures during apoptosis.
Answer: False
Explanation: Caspases are proteases, meaning they degrade proteins. They are the primary executioners of apoptosis, dismantling cellular structures by cleaving key cellular substrates.
Initiator caspases are activated by executioner caspases to begin the apoptotic process.
Answer: False
Explanation: The sequence is reversed: initiator caspases (e.g., caspase-8, caspase-9) are activated first by apoptotic signals, and they subsequently activate executioner caspases (e.g., caspase-3, caspase-7) to carry out the dismantling of the cell.
The Bcl-2 family proteins exclusively promote apoptosis.
Answer: False
Explanation: The Bcl-2 family comprises both pro-apoptotic (e.g., Bax, Bak) and anti-apoptotic (e.g., Bcl-2, Bcl-xL) members. The balance between these proteins critically regulates the intrinsic apoptotic pathway, primarily by controlling mitochondrial outer membrane permeability.
The apoptosome is formed when caspase-3 binds to Apaf-1 and cytochrome c.
Answer: False
Explanation: The apoptosome is a multiprotein complex formed when cytochrome c binds to Apaf-1 in the presence of ATP. This complex then recruits and activates caspase-9, an initiator caspase, not caspase-3 (an executioner caspase).
Inhibitor of Apoptosis Proteins (IAPs) actively promote caspase activation.
Answer: False
Explanation: Inhibitor of Apoptosis Proteins (IAPs) function as negative regulators of apoptosis by directly binding to and inhibiting caspases, thereby preventing their activation and activity.
The discovery of the BCL2 gene's role in inhibiting cell death was crucial for understanding the link between apoptosis dysregulation and cancer.
Answer: True
Explanation: The identification of BCL2 as an inhibitor of apoptosis was a pivotal moment, establishing a direct molecular link between apoptosis dysregulation and cancer development, thereby galvanizing research in the field.
What critical role do Bax and Bak proteins play in the intrinsic apoptotic pathway?
Answer: They form pores in the outer mitochondrial membrane, facilitating cytochrome c release.
Explanation: Bax and Bak are key effectors of the intrinsic pathway, inducing mitochondrial outer membrane permeabilization, which leads to the release of cytochrome c and subsequent activation of the caspase cascade.
What is the function of SMACs released during apoptosis?
Answer: To bind and inhibit Inhibitor of Apoptosis Proteins (IAPs).
Explanation: SMACs (Second Mitochondria-derived Activators of Caspases) are released from mitochondria and counteract the inhibitory function of IAPs, thereby promoting caspase activation and facilitating apoptosis.
What is the primary role of caspases in the apoptotic process?
Answer: To degrade key cellular proteins and dismantle the cell.
Explanation: Caspases are cysteine proteases that act as the central executioners of apoptosis, cleaving numerous cellular substrates to dismantle the cell in a controlled manner.
Which of the following are classified as executioner caspases?
Answer: Caspase-3 and Caspase-7
Explanation: Caspase-3 and Caspase-7 are the principal executioner caspases, responsible for cleaving numerous cellular substrates to execute the apoptotic program after being activated by initiator caspases.
The Bcl-2 family of proteins regulates apoptosis primarily by:
Answer: Influencing mitochondrial membrane permeability.
Explanation: The Bcl-2 family proteins, through their interactions at the mitochondrial membrane, dictate whether the intrinsic apoptotic pathway is activated, primarily by controlling the release of cytochrome c.
Which protein, released from mitochondria, can mediate apoptosis independently of the caspase cascade?
Answer: AIF (Apoptosis-Inducing Factor)
Explanation: Apoptosis-Inducing Factor (AIF) is released from mitochondria during certain apoptotic stimuli and can translocate to the nucleus to induce DNA fragmentation and chromatin condensation in a caspase-independent manner.
The intrinsic pathway of apoptosis is activated by external signals binding to cell-surface death receptors.
Answer: False
Explanation: This describes the extrinsic pathway. The intrinsic pathway is primarily activated by intracellular signals, such as cellular stress, DNA damage, or growth factor withdrawal, leading to mitochondrial dysfunction.
In the intrinsic apoptotic pathway, cytochrome c is released from the cytoplasm into the mitochondria to initiate the caspase cascade.
Answer: False
Explanation: Cytochrome c is normally located within the mitochondrial intermembrane space. In the intrinsic pathway, it is released from the mitochondria into the cytoplasm, where it participates in the formation of the apoptosome.
The extrinsic pathway of apoptosis begins with intracellular signals causing mitochondrial stress.
Answer: False
Explanation: This describes the intrinsic pathway. The extrinsic pathway is initiated by extracellular signals, specifically ligands binding to cell-surface death receptors, leading to the formation of the Death-Inducing Signaling Complex (DISC).
A caspase-independent pathway for apoptosis exists, mediated by proteins like AIF.
Answer: True
Explanation: Indeed, certain proteins such as AIF (Apoptosis-Inducing Factor) can induce cell death through mechanisms that do not involve the canonical caspase cascade, representing a distinct apoptotic pathway.
Tumor Necrosis Factor-alpha (TNF-alpha) is an example of an intracellular signal that triggers the extrinsic apoptotic pathway.
Answer: False
Explanation: TNF-alpha is a cytokine that acts as an extracellular ligand, binding to cell-surface receptors (TNFR1) to initiate the extrinsic apoptotic pathway. It is not an intracellular signal.
The Fas receptor binds to intracellular ligands to initiate apoptosis.
Answer: False
Explanation: The Fas receptor is a cell-surface transmembrane protein that binds to its extracellular ligand, Fas Ligand (FasL), to initiate the extrinsic apoptotic pathway via DISC formation.
In Type I cells undergoing Fas-mediated apoptosis, mitochondrial amplification is essential for caspase activation.
Answer: False
Explanation: Type I cells activate caspases directly from the Fas-DISC, without requiring significant amplification through the mitochondrial pathway. This amplification is characteristic of Type II cells.
Which pathway of apoptosis is initiated by intracellular signals such as cell stress?
Answer: The intrinsic (mitochondrial) pathway
Explanation: The intrinsic pathway, also known as the mitochondrial pathway, is triggered by intracellular stimuli such as DNA damage, oxidative stress, or growth factor deprivation, leading to changes in mitochondrial membrane permeability.
Which component is essential for the formation of the apoptosome in the intrinsic pathway?
Answer: Cytochrome c
Explanation: Cytochrome c, released from mitochondria during intrinsic pathway activation, is a crucial component that binds to Apaf-1 to assemble the apoptosome, which then activates caspase-9.
The extrinsic pathway of apoptosis is typically initiated by:
Answer: Ligands binding to cell-surface death receptors.
Explanation: The extrinsic pathway is triggered when specific extracellular ligands, such as TNF-alpha or FasL, bind to their cognate death receptors on the cell surface, initiating the formation of the DISC.
What is the role of the Fas receptor in the extrinsic apoptotic pathway?
Answer: It is a cell-surface receptor that binds Fas Ligand, initiating DISC formation.
Explanation: The Fas receptor (CD95/Apo-1) is a transmembrane protein that, upon binding Fas Ligand (FasL), recruits adaptor proteins and initiator caspases to form the DISC, thereby initiating the extrinsic apoptotic cascade.
What distinguishes Type I cells from Type II cells in Fas-mediated apoptosis?
Answer: Type I cells activate caspases directly, while Type II cells require mitochondrial amplification.
Explanation: In Type I cells, the Fas-DISC efficiently activates caspases directly. In Type II cells, the initial DISC signal is weaker, necessitating amplification via mitochondrial release of pro-apoptotic factors to achieve robust caspase activation.
Overexpression of anti-apoptotic proteins like XIAP can contribute to cancer development by preventing the death of damaged cells.
Answer: True
Explanation: The sustained survival of cells with accumulated genetic damage, facilitated by the overexpression of anti-apoptotic factors like XIAP, is a critical mechanism contributing to tumor initiation and progression.
The p53 protein promotes cell survival by always initiating DNA repair mechanisms after damage.
Answer: False
Explanation: While p53 can initiate DNA repair, its critical role in response to severe or irreparable damage is to induce apoptosis, thereby eliminating potentially cancerous cells. It does not *always* promote survival.
Human Papillomavirus (HPV) proteins E6 and E7 inhibit apoptosis by activating p53 and retinoblastoma proteins.
Answer: False
Explanation: HPV E6 protein targets p53 for degradation, thereby inhibiting its function. E7 protein binds to and inactivates retinoblastoma proteins. Both actions contribute to uncontrolled cell proliferation and evasion of apoptosis.
Hyperactive apoptosis, or excessive programmed cell death, is implicated in the progression of neurodegenerative diseases like Alzheimer's.
Answer: True
Explanation: Excessive or dysregulated apoptosis contributes to the loss of neurons observed in neurodegenerative conditions such as Alzheimer's and Parkinson's disease.
HIV infection leads to the *increase* of CD4+ T-helper lymphocytes through apoptosis.
Answer: False
Explanation: HIV infection leads to the *depletion* of CD4+ T-helper lymphocytes, partly through mechanisms that induce apoptosis in these critical immune cells.
Viruses often encode proteins that inhibit apoptosis to ensure the survival and replication of the infected host cell.
Answer: True
Explanation: Many viruses have evolved strategies to evade host cell death pathways, including encoding proteins that interfere with apoptosis, thereby prolonging the viability of the infected cell for viral replication and propagation.
Programmed cell death in plants involves phagocytic cells clearing cellular debris, similar to animals.
Answer: False
Explanation: Plants lack specialized phagocytic cells and immune systems for debris clearance. Their programmed cell death mechanisms rely on internal processes, such as vacuole rupture and enzymatic degradation, to manage cellular remnants.
Efferocytosis is the process where cells engulf apoptotic bodies, preventing inflammation.
Answer: True
Explanation: Efferocytosis is the critical process by which phagocytes recognize and engulf apoptotic cells or bodies, ensuring their efficient removal without triggering an inflammatory response.
Phosphatidylserine exposure on the cell surface during apoptosis serves as a signal for cell proliferation.
Answer: False
Explanation: Phosphatidylserine exposure on the outer leaflet of the plasma membrane during apoptosis acts as an 'eat me' signal, marking the cell for recognition and engulfment by phagocytes, not for proliferation.
SMACs are proteins that promote apoptosis by activating Inhibitor of Apoptosis Proteins (IAPs).
Answer: False
Explanation: SMACs (Second Mitochondria-derived Activators of Caspases) promote apoptosis by binding to and antagonizing the inhibitory function of IAPs, thereby allowing caspases to become active.
Nitric oxide (NO) exclusively induces apoptosis by increasing mitochondrial membrane potential.
Answer: False
Explanation: Nitric oxide (NO) has a complex role in apoptosis; it can induce apoptosis by affecting mitochondrial membrane potential, but it can also inhibit apoptosis or promote cell survival depending on the cellular context and concentration.
Excessive apoptosis (hyperactive apoptosis) is implicated in which group of diseases?
Answer: Neurodegenerative diseases and HIV infection.
Explanation: Hyperactive apoptosis contributes to tissue atrophy and cell loss in conditions such as neurodegenerative disorders (e.g., Alzheimer's, Parkinson's) and immune deficiency states like AIDS, characterized by the depletion of CD4+ T-cells.
How does HIV infection contribute to the depletion of CD4+ T-helper lymphocytes?
Answer: By interfering with anti-apoptotic proteins and activating pro-apoptotic pathways, leading to apoptosis.
Explanation: HIV pathogenesis involves mechanisms that disrupt the normal balance of apoptosis regulation in CD4+ T-cells, leading to their premature death and contributing to immune system collapse.
Viruses can manipulate apoptosis for their benefit by:
Answer: Encoding proteins that inhibit apoptosis to prolong host cell survival.
Explanation: Many viruses encode proteins that interfere with host cell apoptosis pathways, thereby extending the lifespan of infected cells to maximize viral replication and assembly.
What is a key difference in programmed cell death mechanisms between plants and animals?
Answer: Plants lack immune systems for debris removal and rely on internal mechanisms like vacuole rupture.
Explanation: Unlike animals, plants do not possess specialized phagocytic cells for clearing apoptotic debris. They employ internal mechanisms, such as vacuole rupture and enzymatic degradation, to manage cell death and its byproducts.
Which of the following viral proteins is an example of a viral homolog that inhibits apoptosis?
Answer: Adenovirus E1B-55K
Explanation: Adenovirus protein E1B-55K is known to interfere with the function of the tumor suppressor p53, thereby inhibiting apoptosis and contributing to viral replication and oncogenesis.
Efferocytosis is the process where cells engulf apoptotic bodies, preventing inflammation.
Answer: True
Explanation: Efferocytosis is the critical process by which phagocytes recognize and engulf apoptotic cells or bodies, ensuring their efficient removal without triggering an inflammatory response.
The 'Warburg hypothesis' suggests that cancer cells often shift their metabolism towards glycolysis, which is sometimes correlated with the pathological inactivation of apoptosis.
Answer: True
Explanation: The Warburg effect, characterized by increased glycolysis even in the presence of oxygen, is frequently observed in cancer cells and is often associated with mechanisms that promote survival by evading apoptosis.
The 'Warburg hypothesis' relates cancer metabolism to apoptosis by suggesting a correlation between:
Answer: Shift towards glycolysis and inactivation of apoptosis.
Explanation: The Warburg hypothesis posits that cancer cells preferentially utilize glycolysis. This metabolic shift is often correlated with the dysregulation or inactivation of apoptotic pathways, contributing to tumor cell survival.
The 'Lock-in and apoptosis' strategy for HIV eradication aims to:
Answer: Induce apoptosis in infected cells by trapping the virus inside.
Explanation: This strategy employs compounds that inhibit viral budding, effectively trapping the virus within infected cells and promoting their subsequent elimination via apoptosis.
What role does the CD4 glycoprotein play in the context of HIV and apoptosis?
Answer: HIV proteins reduce CD4 glycoprotein levels, contributing to T-cell apoptosis.
Explanation: HIV infection often leads to a reduction in CD4 glycoprotein expression on T-helper cells, which is associated with the induction of apoptosis and subsequent depletion of these vital immune cells.
How does Canine Distemper Virus (CDV) induce apoptosis in HeLa cells, according to the source?
Answer: Via the intrinsic pathway, bypassing caspase-8.
Explanation: Studies indicate that Canine Distemper Virus (CDV) induces apoptosis in HeLa cells through the intrinsic pathway, notably bypassing the activation of caspase-8, which is typically involved in the extrinsic pathway.
Therapeutic strategies targeting apoptosis aim solely to induce cell death in diseased cells.
Answer: False
Explanation: Therapeutic strategies can aim to either induce apoptosis (e.g., in cancer) or inhibit apoptosis (e.g., in neurodegenerative diseases or during ischemia), depending on the pathological context.
Gene knockouts are primarily used to observe the effects of gene overexpression in apoptosis pathways.
Answer: False
Explanation: Gene knockouts are employed to *inactivate* specific genes, thereby allowing researchers to study the physiological consequences of their absence and elucidate their roles in biological processes like apoptosis.
Which of the following is a therapeutic strategy aimed at *inducing* apoptosis in cancer cells?
Answer: Administering Smac mimetics.
Explanation: Smac mimetics are designed to antagonize IAPs, thereby promoting caspase activation and inducing apoptosis, making them a strategy for cancer therapy. Blocking survival pathways also induces apoptosis, but Smac mimetics directly target the apoptotic machinery.
How are gene knockouts utilized in studying apoptosis pathways?
Answer: To observe the effects of inactivating specific genes.
Explanation: Gene knockouts are a fundamental tool in molecular biology that allow researchers to determine the function of a gene by observing the phenotypic consequences of its absence, crucial for dissecting complex pathways like apoptosis.
What is the significance of DNA laddering in apoptosis research?
Answer: It represents the fragmentation of DNA into specific sizes, characteristic of apoptosis.
Explanation: DNA laddering, visualized as distinct bands on an electrophoresis gel, signifies the specific cleavage of DNA into fragments corresponding to nucleosomal units, a key biochemical hallmark of apoptosis.
How can defects in apoptotic pathways contribute to cancer?
Answer: By allowing damaged or abnormal cells to survive and proliferate.
Explanation: The evasion of apoptosis is a critical hallmark of cancer, enabling cells with oncogenic mutations and DNA damage to survive, proliferate, and accumulate further genetic alterations, ultimately leading to tumor formation.
What is the primary function of the p53 protein in response to severe DNA damage?
Answer: To halt the cell cycle and promote DNA repair, or induce apoptosis if repair is impossible.
Explanation: The tumor suppressor p53 acts as a critical checkpoint regulator; it can arrest the cell cycle to allow for DNA repair or, if damage is too extensive, trigger apoptosis to eliminate the compromised cell.
HPV proteins E6 and E7 contribute to the immortality of cells like HeLa by:
Answer: Inhibiting p53 and binding retinoblastoma proteins.
Explanation: HPV E6 and E7 proteins subvert cellular control mechanisms by inactivating key tumor suppressors like p53 and retinoblastoma proteins, thereby promoting uncontrolled proliferation and resistance to apoptosis.
Which of the following is a therapeutic strategy aimed at *inducing* apoptosis in cancer cells?
Answer: Administering Smac mimetics.
Explanation: Smac mimetics are designed to antagonize IAPs, thereby promoting caspase activation and inducing apoptosis, making them a strategy for cancer therapy. Blocking survival pathways also induces apoptosis, but Smac mimetics directly target the apoptotic machinery.
The 'Lock-in and apoptosis' strategy for HIV eradication involves using compounds to promote viral budding.
Answer: False
Explanation: This strategy utilizes compounds that suppress viral budding, thereby trapping the virus within infected cells and promoting their subsequent elimination via apoptosis, rather than promoting budding.
The 'Lock-in and apoptosis' strategy for HIV eradication aims to:
Answer: Induce apoptosis in infected cells by trapping the virus inside.
Explanation: This strategy employs compounds that inhibit viral budding, effectively trapping the virus within infected cells and promoting their subsequent elimination via apoptosis.
What are some methods used to distinguish between apoptotic and necrotic cells?
Answer: Assessing cell membrane integrity and morphology.
Explanation: Distinguishing between apoptosis and necrosis involves evaluating morphological changes (e.g., cell shrinkage vs. swelling), membrane integrity (phosphatidylserine exposure in apoptosis, loss of integrity in necrosis), and biochemical markers like caspase activation.
Programmed cell death in plants involves phagocytic cells clearing cellular debris, similar to animals.
Answer: False
Explanation: Plants lack specialized phagocytic cells for debris clearance. Their programmed cell death mechanisms rely on internal processes, such as vacuole rupture and enzymatic degradation, to manage cellular remnants.
What is a key difference in programmed cell death mechanisms between plants and animals?
Answer: Plants lack immune systems for debris removal and rely on internal mechanisms like vacuole rupture.
Explanation: Unlike animals, plants do not possess specialized phagocytic cells for clearing apoptotic debris. They employ internal mechanisms, such as vacuole rupture and enzymatic degradation, to manage cell death and its byproducts.