Apoptosis
54 flashcards covering Apoptosis for the MCAT Biology & Biochemistry section.
Apoptosis is a controlled process of programmed cell death that helps maintain the body's balance by eliminating damaged or unnecessary cells. Unlike accidental cell death, which is chaotic and inflammatory, apoptosis occurs in an orderly manner, involving specific molecular signals that lead to cell shrinkage, DNA fragmentation, and eventual breakdown. This process is crucial for normal development, such as shaping fingers in embryos, and for preventing diseases like cancer by removing abnormal cells.
On the MCAT, apoptosis frequently appears in biology and biochemistry questions, often in passage-based scenarios or discrete items testing your understanding of cellular mechanisms. You'll encounter questions on pathways like the intrinsic (mitochondrial) and extrinsic (death receptor) routes, as well as comparisons to necrosis—a common trap where students confuse the two based on symptoms. Focus on key regulators, such as caspases and Bcl-2 proteins, and their roles in disease. For success, always link apoptosis to its clinical implications. Remember to distinguish it from necrosis by noting apoptosis's non-inflammatory nature.
Terms (54)
- 01
Apoptosis
Apoptosis is a genetically programmed process of controlled cell death that eliminates unwanted or damaged cells without causing inflammation, playing a key role in development and maintaining tissue homeostasis.
- 02
Programmed Cell Death
Programmed cell death refers to the orderly dismantling of cells as directed by genetic instructions, with apoptosis being the primary form that ensures cells die quietly and are efficiently removed.
- 03
Intrinsic Apoptotic Pathway
The intrinsic apoptotic pathway is triggered by internal signals like DNA damage, involving mitochondrial outer membrane permeabilization and the release of cytochrome c to activate caspases.
- 04
Extrinsic Apoptotic Pathway
The extrinsic apoptotic pathway is initiated by external signals binding to death receptors on the cell surface, such as Fas ligand binding to Fas, which activates caspase-8 and leads to cell death.
- 05
Caspases
Caspases are a family of protease enzymes that play essential roles in apoptosis by cleaving specific proteins, with initiator caspases activating executioner caspases to dismantle the cell.
- 06
Initiator Caspases
Initiator caspases, such as caspase-8 and caspase-9, are activated early in the apoptotic pathways and then cleave and activate executioner caspases to propagate the cell death process.
- 07
Executioner Caspases
Executioner caspases, like caspase-3 and caspase-7, are activated by initiator caspases and directly degrade cellular components, leading to the morphological changes seen in apoptosis.
- 08
Bcl-2 Family Proteins
The Bcl-2 family proteins regulate the intrinsic apoptotic pathway by controlling mitochondrial membrane permeability, with pro-apoptotic members like Bax promoting cytochrome c release and anti-apoptotic ones like Bcl-2 inhibiting it.
- 09
Cytochrome c
Cytochrome c is a protein released from mitochondria during the intrinsic apoptotic pathway, which forms the apoptosome and activates caspase-9, amplifying the cell death signal.
- 10
Apoptosome
The apoptosome is a multi-protein complex formed by cytochrome c and Apaf-1 that activates caspase-9, serving as a critical step in the intrinsic pathway to commit the cell to apoptosis.
- 11
p53 and Apoptosis
p53 is a tumor suppressor protein that promotes apoptosis in response to DNA damage by upregulating genes like Bax, which triggers the intrinsic pathway to eliminate potentially cancerous cells.
- 12
Death Receptors
Death receptors are cell surface proteins, such as Fas and TNFR1, that belong to the TNF receptor family and initiate the extrinsic apoptotic pathway upon binding to their ligands.
- 13
Fas Ligand
Fas ligand is a protein that binds to the Fas death receptor, triggering the extrinsic apoptotic pathway and leading to the activation of caspase-8 in immune cells to induce cell death.
- 14
Mitochondrial Outer Membrane Permeabilization
Mitochondrial outer membrane permeabilization is a key event in the intrinsic apoptotic pathway where pro-apoptotic proteins form pores, releasing cytochrome c into the cytosol.
- 15
DNA Fragmentation
DNA fragmentation is a hallmark of apoptosis where endonucleases cleave DNA into nucleosome-sized pieces, resulting in the characteristic laddering pattern on gel electrophoresis.
- 16
Membrane Blebbing
Membrane blebbing is a morphological change in apoptosis where the cell membrane forms bubble-like protrusions due to cytoskeletal disruption, aiding in the packaging of cellular contents.
- 17
Phagocytosis of Apoptotic Cells
Phagocytosis of apoptotic cells involves macrophages recognizing and engulfing dying cells without inflammation, preventing tissue damage and maintaining homeostasis.
- 18
Role of Apoptosis in Development
Apoptosis plays a crucial role in embryonic development by sculpting tissues, such as removing webbing between fingers and toes, to form proper structures.
- 19
Apoptosis in Immune System
In the immune system, apoptosis eliminates self-reactive lymphocytes during development and removes activated immune cells after infection to prevent autoimmunity and maintain tolerance.
- 20
Apoptosis and Cancer
Apoptosis acts as a defense against cancer by eliminating cells with DNA damage, but cancer cells often evade it through mutations in genes like p53, allowing uncontrolled growth.
- 21
Inhibitors of Apoptosis
Inhibitors of apoptosis, such as Bcl-2 proteins, prevent cell death by blocking mitochondrial permeabilization or caspase activation, which can contribute to cancer if overexpressed.
- 22
Apoptotic Signals
Apoptotic signals include internal stressors like DNA damage and external cues like death ligands, which activate pathways leading to caspase activation and cell dismantling.
- 23
Caspase Cascade
The caspase cascade is a sequential activation of proteases where initiator caspases activate executioner caspases, amplifying the apoptotic signal for efficient cell death.
- 24
Pro-apoptotic Proteins
Pro-apoptotic proteins, such as Bax and Bak, promote cell death by inducing mitochondrial membrane permeabilization and cytochrome c release in the intrinsic pathway.
- 25
Anti-apoptotic Proteins
Anti-apoptotic proteins, like Bcl-2 and Bcl-xL, inhibit apoptosis by preventing the activation of pro-apoptotic proteins and maintaining mitochondrial integrity.
- 26
Apoptotic Bodies
Apoptotic bodies are membrane-bound vesicles containing cellular fragments that form during apoptosis, allowing for safe removal by phagocytes without leaking contents.
- 27
Autophagy vs. Apoptosis
Autophagy is a survival mechanism that recycles cellular components, whereas apoptosis is a cell death process; they can intersect, but apoptosis leads to complete dismantling.
- 28
Anoikis
Anoikis is a form of apoptosis triggered by inadequate cell-matrix interactions, such as when cells detach from the extracellular matrix, preventing metastasis in normal tissues.
- 29
Endonuclease Activation
Endonuclease activation in apoptosis leads to DNA cleavage, a key step that results in the fragmentation necessary for the orderly disposal of the cell's genetic material.
- 30
Chromatin Condensation
Chromatin condensation is an early event in apoptosis where the nucleus compacts, making DNA more accessible for fragmentation and aiding in the cell's silent demise.
- 31
Cell Shrinkage in Apoptosis
Cell shrinkage in apoptosis occurs due to water loss and cytoskeletal breakdown, distinguishing it from necrotic swelling and facilitating the cell's removal.
- 32
Pyknosis
Pyknosis is the irreversible condensation of chromatin in apoptotic cells, appearing as a shrunken, darkened nucleus under microscopy.
- 33
Karyorrhexis
Karyorrhexis is the fragmentation of the nucleus during apoptosis, following chromatin condensation, which breaks DNA into pieces for eventual clearance.
- 34
Necrosis vs. Apoptosis
Necrosis is accidental cell death caused by injury, leading to inflammation, whereas apoptosis is controlled and non-inflammatory, preserving tissue integrity.
- 35
Inflammation in Necrosis
In necrosis, cell lysis releases contents that trigger inflammation, unlike apoptosis where cells are packaged to avoid immune activation.
- 36
ATP Dependence in Apoptosis
Apoptosis requires ATP for processes like caspase activation and DNA fragmentation, making it an energy-dependent form of cell death, unlike rapid necrosis.
- 37
Common Triggers of Apoptosis
Common triggers of apoptosis include DNA damage, growth factor withdrawal, and viral infections, which activate pathways to eliminate compromised cells.
- 38
DNA Damage and Apoptosis
DNA damage can induce apoptosis via p53 activation, ensuring that cells with irreparable genetic errors are removed to prevent mutations from persisting.
- 39
Hypoxia and Apoptosis
Hypoxia, or low oxygen, can trigger apoptosis in cells through the intrinsic pathway, helping to eliminate cells in ischemic tissues.
- 40
Growth Factor Withdrawal
Growth factor withdrawal initiates apoptosis by activating pro-apoptotic signals, as seen in cells that lose survival signals, leading to programmed death.
- 41
TNF-alpha Signaling
TNF-alpha signaling through its receptor activates the extrinsic apoptotic pathway, promoting cell death in immune responses or in response to infection.
- 42
Phagocytic Recognition
Phagocytic recognition of apoptotic cells involves surface changes like phosphatidylserine exposure, allowing macrophages to engulf them without inflammation.
- 43
Apoptosis in Neural Development
Apoptosis in neural development removes excess neurons, refining connections and ensuring proper brain function through programmed cell elimination.
- 44
Evasion of Apoptosis in Cancer
Evasion of apoptosis in cancer occurs when mutations disable pathways like p53, allowing tumor cells to survive and proliferate unchecked.
- 45
Strategy for Distinguishing Apoptosis and Necrosis
To distinguish apoptosis and necrosis, look for controlled DNA fragmentation and no inflammation in apoptosis versus cell swelling and immune response in necrosis.
- 46
Example of Apoptosis in Tadpole Tail Resorption
In tadpole metamorphosis, apoptosis resorbs the tail as the organism transitions to a frog, demonstrating its role in developmental remodeling.
During tadpole development, cells in the tail undergo apoptosis, leading to its gradual disappearance.
- 47
Apoptosis in Webbed Finger Regression
Apoptosis drives the regression of webbed fingers in human embryos by selectively eliminating cells between digits, shaping the hand structure.
In fetal development, interdigital cells die via apoptosis, separating the fingers.
- 48
Viral Inhibition of Apoptosis
Viruses inhibit apoptosis to prolong host cell survival for replication, using proteins that block caspases or mimic anti-apoptotic factors.
- 49
Chemotherapy and Apoptosis
Chemotherapy induces apoptosis in cancer cells by causing DNA damage, relying on the intrinsic pathway to trigger cell death and shrink tumors.
- 50
Radiation Therapy and Apoptosis
Radiation therapy triggers apoptosis in cancer cells through DNA damage and p53 activation, aiming to eliminate malignant cells while sparing healthy ones.
- 51
Endogenous vs. Exogenous Pathways
Endogenous pathways of apoptosis are internally triggered, like the intrinsic mitochondrial pathway, while exogenous ones are externally signaled, like the extrinsic receptor pathway.
- 52
Feedback Loops in Apoptosis
Feedback loops in apoptosis, such as caspase activation enhancing further caspase activity, amplify the death signal to ensure complete and irreversible cell dismantling.
- 53
Bcl-2 Overexpression in Cancer
Bcl-2 overexpression in cancer cells inhibits apoptosis by preventing mitochondrial cytochrome c release, contributing to tumor survival and resistance to treatment.
- 54
DNA Laddering
DNA laddering is the electrophoretic pattern of fragmented DNA in apoptosis, resulting from endonuclease activity and serving as a diagnostic marker.