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Magazine Chapter 21: Problem 14
Based on your understanding of the events surrounding cell death, predict the effect(s) of the following on the ability of a cell to undergo apoptosis: a. Functional CED-9; nonfunctional CED-3 b. Active Bax and cytochrome \(c ;\) nonfunctional caspase- 9 c. Inactive PI-3 kinase; active Bad
Short Answer
Expert verified
a) Apoptosis is inhibited; b) Apoptosis is blocked; c) Apoptosis proceeds.
Step by step solution
01
Understand the role of CED-9 and CED-3 in apoptosis
CED-9 is an anti-apoptotic protein that inhibits apoptosis, while CED-3 is a pro-apoptotic protease crucial for the execution phase of apoptosis. For apoptosis to proceed, CED-3 must be functional to cleave cellular components necessary for cell death.
02
Analyze the effect of functional CED-9 and nonfunctional CED-3 (Scenario a)
With functional CED-9, the apoptotic process is inhibited from the beginning. Even if CED-9 action was ineffective, a nonfunctional CED-3 prevents the execution of apoptosis since it cannot cleave downstream proteins needed for cell death.
03
Understand the roles of Bax, cytochrome c, and caspase-9
Bax promotes the release of cytochrome c from mitochondria, which then helps activate caspase-9, an initiator caspase that triggers downstream executioner caspases in apoptosis.
04
Analyze the effect of active Bax, cytochrome c, and nonfunctional caspase-9 (Scenario b)
Though Bax can release cytochrome c, a nonfunctional caspase-9 means that the apoptosome formation and subsequent activation of executioner caspases like caspase-3 cannot occur, thus blocking apoptosis at this stage.
05
Understand the roles of PI-3 kinase and Bad in apoptosis regulation
PI-3 kinase promotes cell survival pathways by activating Akt, which inactivates Bad, a pro-apoptotic member of the Bcl-2 family, through phosphorylation.
06
Analyze the effect of inactive PI-3 kinase and active Bad (Scenario c)
Without active PI-3 kinase, the Akt pathway does not inhibit Bad because Bad remains dephosphorylated and active. Active Bad promotes apoptosis by inhibiting anti-apoptotic proteins like Bcl-2, thus promoting apoptosis.
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Key Concepts
These are the key concepts you need to understand to accurately answer the question.
CED-9 protein
The CED-9 protein is an essential player in the regulation of apoptosis, the programmed cell death that occurs in multicellular organisms. CED-9 acts as an anti-apoptotic factor, meaning it helps prevent the cell from undergoing apoptosis. It is similar to the Bcl-2 protein found in mammals and helps maintain cell survival by inhibiting other proteins that promote apoptosis.
CED-9 achieves this by binding to apoptotic proteins and preventing them from acting.
CED-9 achieves this by binding to apoptotic proteins and preventing them from acting.
- CED-9 inhibits the apoptotic pathway at its early stages.
- In scenarios where CED-9 is functional, apoptosis is generally blocked, as it prevents the activation of downstream pro-apoptotic factors like CED-3.
CED-3 protein
CED-3 protein plays a pivotal role in apoptosis as a pro-apoptotic protease. It is comparable to caspases in humans, specifically caspase-3, and is crucial for executing apoptosis. CED-3 is produced in the cell as an inactive precursor or zymogen, which is only activated when apoptosis is necessary.
Upon activation, CED-3 cleaves specific cellular components, leading to the dismantling of the cell.
Upon activation, CED-3 cleaves specific cellular components, leading to the dismantling of the cell.
- CED-3 acts downstream of CED-9 in the apoptotic pathway.
- It is essential for the execution phase of apoptosis.
Caspase-9
Caspase-9 is an important component of the intrinsic apoptosis pathway, acting as an initiator caspase. It is a human homolog of the CED-3 protein in nematodes. Caspase-9 becomes active in response to apoptotic signals that originate from within the cell, often due to cellular stress or damage.
It forms part of the apoptosome complex, which includes cytochrome c and Apaf-1, and this complex is crucial for the activation of executioner caspases like caspase-3.
It forms part of the apoptosome complex, which includes cytochrome c and Apaf-1, and this complex is crucial for the activation of executioner caspases like caspase-3.
- Caspase-9 activation is essential for advancing the apoptosis signals to the execution phase.
- If caspase-9 is nonfunctional, even if cytochrome c is released and Bax is activated, apoptosis is halted as downstream caspases remain inactive.
PI-3 kinase
PI-3 kinase plays a significant role in cell survival pathways, acting to promote cell growth and survival. It does this by activating a protein kinase known as Akt, which further signals to inhibit processes that would lead to apoptosis.
When PI-3 kinase is activated, Akt phosphorylates and inactivates pro-apoptotic factors such as Bad.
When PI-3 kinase is activated, Akt phosphorylates and inactivates pro-apoptotic factors such as Bad.
- PI-3 kinase helps cells survive in potentially harmful environments by reinforcing anti-apoptotic signals.
- In the absence of PI-3 kinase activity, Bad remains active, which can incline the cell towards apoptosis as Bad inhibits anti-apoptotic proteins in the Bcl-2 family.
Bax
Bax is a pro-apoptotic member of the Bcl-2 protein family, which plays a pivotal role in regulating apoptosis. It is primarily involved in the mitochondrial or intrinsic pathway of apoptosis. Bax promotes apoptosis by facilitating the release of cytochrome c from the mitochondria into the cytoplasm.
Once cytochrome c is released, it can trigger the formation of the apoptosome, thereby activating caspase-9.
Once cytochrome c is released, it can trigger the formation of the apoptosome, thereby activating caspase-9.
- The activation of Bax can occur due to various intrinsic cellular stresses, such as DNA damage.
- In the presence of active Bax, pro-apoptotic signals are amplified, pushing the cell towards apoptosis.
Cytochrome c
Cytochrome c is an important molecule in the intrinsic pathway of apoptosis. It is usually located in the mitochondrial intermembrane space and plays a crucial role in cellular energy production under normal conditions.
During apoptosis, however, cytochrome c is released into the cytoplasm as part of the cellular response to stress or damage. Once in the cytoplasm, cytochrome c associates with Apaf-1 and caspase-9 to form the apoptosome.
During apoptosis, however, cytochrome c is released into the cytoplasm as part of the cellular response to stress or damage. Once in the cytoplasm, cytochrome c associates with Apaf-1 and caspase-9 to form the apoptosome.
- This complex initiates the cascade of caspase activation leading to apoptosis.
- The release of cytochrome c is one of the early events in the apoptosis cascade, particularly following Bax activation.
Bad protein
The Bad protein is a pro-apoptotic member of the Bcl-2 family, which plays a crucial role in regulating cell survival and apoptosis. Under normal conditions, Bad promotes apoptosis by binding to anti-apoptotic proteins such as Bcl-2 and Bcl-xL, inhibiting their function.
However, in the presence of survival signals, Bad becomes phosphorylated by Akt鈥攁 process promoted by PI-3 kinase鈥攁nd is sequestered in the cytoplasm via association with 14-3-3 proteins, rendering it inactive.
However, in the presence of survival signals, Bad becomes phosphorylated by Akt鈥攁 process promoted by PI-3 kinase鈥攁nd is sequestered in the cytoplasm via association with 14-3-3 proteins, rendering it inactive.
- When Bad is unphosphorylated, it promotes apoptosis by freeing Bax and Bak to permeabilize the mitochondrial membrane.
- In conditions where PI-3 kinase is inactive or Akt signaling is disrupted, Bad remains active and can contribute to the initiation of apoptosis.
