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Pathogenic Microbiology > Lecture 7: APOPTOSIS AND TUMOR SUPPRESSION > Flashcards

Lecture 7: APOPTOSIS AND TUMOR SUPPRESSION Flashcards

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1
Q

What is apoptosis?

A

Cell’s own molecules are ultimately responsible for its death

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2
Q

What is necrosis?

A

The cell is a victim of molecules synthesized by other cells; for example, necrosis results from the effects of toxic molecules on a cell.

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3
Q

What is Pyroptosis?

A

It is highly inflammatory and is in response to some intracellular pathogens or non-infectious stimuli. Pyroptosis is a caspase-1 dependent process that results in the release of the inflammatory cytokines IL-18 and IL-1β.

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4
Q

How does tumor-supressor gene keep cell numbers down?

A

Tumor-suppressor genes keep cell numbers down, either

  1. by inhibiting progress through the cell cycle and thereby preventing cell birth particles or
  2. by promoting programmed cell death (also called apoptosis).
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5
Q

What happens tumor-suppressor genes are rendered non-functional?

A

When cellular tumor suppressor genes are rendered non-functional through mutation, the cell becomes malignant. One example is the p53 gene, which inhibits cyclin-dependent kinases and is inactivated in many different tumors.

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6
Q

What does oncogenes stimulate?

A

Oncogenes stimulate appropriate cell growth under normal conditions, as required for the continued turnover and replenishment of the skin, gastrointestinal tract, and blood

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7
Q

What is an example of mutant oncogenes?

A

Ras, activated in pancreatic and colon cancers
Bcl-2, activated in lymphoid tumors. Amplification of oncogenes (more than their normal gene copy number) is also found in cancer: e.g., MDM2 is amplified in liposarcomas.

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8
Q

What are characteristics of BCL2/BCL-xl?

A

Transmembrane protein
contains Bcl-2 Homology (BH) domains BH1-4
Localizes to outer mitochondrial membrane, ER, perinuclear membrane, but not plasma membrane.
Heterodimerizes with pro-apoptotic family members such as Bax

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9
Q

What is the purpose of BCL-2/BCL-xL?

A

Functions to repress many, but not all, apoptotic pathways
serves as a pro survival function by preventing the release of mitochondrial contents such as cytochrome c that would lead to caspase activation

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10
Q

What happens when we have too much MDM2?

A

Too much MDM2 can cause cancer because it inhibits p53 which prevents cell death

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11
Q

What are the 2 classes of Caspases?

A

Initiators

Effectors (excutioners)

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12
Q

What are features of Caspases?

A

The initiation of the cascade reaction is regulated by caspase inhibitors.
All caspases have a similar domain structure
Not all mammalian caspases participate in apoptosis: For example, Caspases 4, 5, and 12 are activated during innate immune responses and are involved in the regulation of the inflammatory response

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13
Q

What is the role of effector caspases?

A

Effector caspases (such as caspase-3, -6 and -7 in mammals) function to breakdown cell structures through cleavage of specific substrates.

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14
Q

What Is the role of IAP Family?

A

they inhibit apoptosis, specifically through binding and inhibiting caspases

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15
Q

Describe the ways apoptosis occurs?

A
  1. Pore-forming
  2. Superantigen, such as enterotoxins from Staphylococcus aureus
  3. Toxins interfere with host signaling (AB toxins )
  4. Some bacterial pathogens use type-III secretion apparatus to deliver a set of effector proteins into the host cytosol
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16
Q

What are ways that microorganisms cause induction of apoptosis?

A
  1. activation of host cell receptors that signal for apoptosis
  2. induction of second messengers
  3. regulation of caspase activity
  4. inhibition of protein synthesis
  5. disruption of cytoplasmic membrane
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17
Q

what is an intrinsic defense mechanism by the host in response to microbial infection?

A

Cell death and infection

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18
Q

What are the examples of cell death mechanisms?

A

apoptosis, necrosis, pyroptosis

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19
Q

what are the two steps in necrosis?

A

from normal cell, it goes to:

  1. irregular chromatin clumping, mitochondria swells
  2. cellular components disintegrate, membrane rupture
20
Q

what are the steps in apoptosis?

A

from normal cell it goes to:

  1. compaction and segregation of chromatin, convolution of nuclear outline
  2. nucleus fragments, cytoplasm condenses, cell surface protusion, membrane bound apoptopic bodies,
  3. phagocytosis of apoptopic bodies
  4. degradation by lysosomal enzymes
  5. digestion within lysosomes
21
Q

what organism was used as a genetic model for determining apoptopic pathways?

A

C. elegans (the worm)

22
Q

Why is the ratio of BCL-2/Bax important?

A

Ratio of Bcl-2:Bax important in determining susceptibility to death

23
Q

What occurs in cells with oncogene mutants?

A

cells with gain-of-function mutant oncogenes continue to grow (or refuse to die) even when they are receiving no growth signals.

24
Q

what is important about BH3?

A

BH3 only proteins bind and regulate the anti-apoptopic BCL-2 proteins to promote apoptosis

25
Q

what in p53 interacts directly with DNA?

A

the central core domain

26
Q

what are the “hot spots” of tumor derived p53 mutations?

A

the amino acid residues in the core domain that are critical for DNA binding

27
Q

what are the two ways p53 induces apoptosis?

A
  1. through transcriptional activation of pro-apoptic genes (such as Puma, Noxa, Bax, Apaf-1)
  2. localization to mitochondria via interaction with Bcl-2 family protein Bcl-xL and facilitating Bax oligomerization
28
Q

What do initiator caspase do?

A

Initiator caspases initiate the caspase cascade by cleaving the inactive forms of the effector caspases (called pro-forms), thereby activating them.
caspase 2, 8-10

29
Q

What do effector caspase do once activated?

A

Once activated, effector caspases in turn cleave other protein substrates to advance the apoptotic process.

30
Q

what does the pro domain of the initiator pro caspase do?

A

recruit other pro caspases to dimerize

31
Q

what do both pro caspases and linker region in the dimer undergo?

A

autocatalysis, where both the pro domain and the linker region between the small and large subunit are cleaved, leading to formation of an active heterotramer

32
Q

How does initiator caspases activate effector caspases?

A

they cleave effector caspases at sites, resulting in production of small and large subunits of the effector caspase

33
Q

what are the cell structures that effector caspases break down?

A

actin cytoskeleton, lamins, golgi, and translation apparatus

34
Q

what is BIR?

A

baculoviral IAP repeat, essential for anti-apoptotic activity, blocks caspases or activation of caspases
Not all BIRP’s are IAPs

35
Q

what happens if ced-9/Bcl-2 lose function?

A

too many cells die

36
Q

what happens if ced3, ced4, or caspases lose function?

A

too many cells live, cancer

37
Q

what are the proteins in pro-survival?

A

Bcl-2 and Bcl-X

38
Q

what are the proteins in pro-apoptosis?

A

Bax and Noxa

39
Q

what consist of the p53 binding sites?

A

four copies of the pentamer consensus sequences

40
Q

what are the oncogenes that regulate p53?

A

E1A, Myc, and Ras promote p53

41
Q

What Kinase promote p53?

A

ATM, Chk2, ATR, casein Kinase II

42
Q

what acetylases from DNA damage regulate p53?

A

PCAF and p300 promote p53

43
Q

what proteins inhibit Bcl-2 and Bcl-xL?

A

Noxa

44
Q

what proteins inhibit apaf-1?

A

Bcl-2 and Bcl-xL

45
Q

what proteins promote Apaf-1?

A

Bax

46
Q

what does Apaf-1 promote?

A

Caspase 9 and 3

47
Q

How are Initiator capses auto-activated?

A
  1. Pro-domain of initiator pro-caspases (such as Caspase 8) recruits other pro-caspases to dimerize.
  2. Both pro-caspases in the dimer undergo autocatalysis where both the pro-domain and the linker region between the large and small subunit are cleaved, leading to the formation of an active heterotetramer.

Pathogenic Microbiology (12 decks)

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