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Molecular Cell Biology > (4) Chapter 18: Cell Death and Cell Renewal > Flashcards

(4) Chapter 18: Cell Death and Cell Renewal Flashcards

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1
Q

Functions of programmed cell death

A
  1. balances cell proliferation
  2. maintains constant cell numbers
  3. eliminates damaged and potentially dangerous cells
  4. eliminates unwanted cells from many tissues during development
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2
Q

Example of elimination of unwanted cells

A
  1. Elimination of larval tissues during amphibian and insect metamorphosis.
  2. elimination of tissue beterrn digits in formation of fingers and toes
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3
Q

Necrosis

A

Accidental cell death from acute injury

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4
Q

Apoptosis

A
  • programmed cell death; an active process

- characterized by DNA fragmentation, chromatin condensation, fragmentation of the nucleus and cell

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5
Q

How are apoptotic cells removed from tissue?

A
  • apoptotic cells and cell fragments are recognized and phagocytosed by macrophages and neighboring cells
  • express “eat me” signals
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6
Q

How do Necrotic decompose?

A

-swell & lyse, contents released into the extracellular space and cause inflammation

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7
Q

Phosphatidylserine

A
  • an “eat me” signal expressed by apoptotic cells

- in normal cells phosphatidylserine is restricted to the inner leaflet of the PM

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8
Q

What are the central regulator and effectors of apoptosis

A

-Ced-9, Ced-4, Ced-3

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9
Q

Ced-3

A

-prototype of caspases family of proteases

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10
Q

Caspases

A
  • The ultimate executioners of programmed cell death

- cleave over 100 different target proteins

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11
Q

How do caspases “execute?”

A
  • have cysteine (C) residues at their active sites and cleave after aspartic acid (ASP) residues in their substrate proteins
  • activation of an initiator caspase starts a chain reaction of caspase activation leading to death of cell
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12
Q

How are caspases synthesized?

A

-as inactive precursors (procaspases) that convert to active forms by proteolytic cleavage, catalyzed by other caspases

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13
Q

How are caspases activated?

A

-activated in response to various signals. THey then cleave and activate effector caspases, which digest the cellular target proteins

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14
Q

ced-9 in C.elegans

A

-related to the mammalian gene bcl-2, which was first identified as an oncogene

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15
Q

Bcl-2

A
  • antiapoptotic protein
  • inhibits apoptosis. Cancer cells are unable to undergo apoptosis
  • mammals encode about 20 proteins related to Bcl-2; some inhibit apoptosis, others induce caspase activation
  • acts at mitochondria and play a central role in controlling programmed cell death
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16
Q

How is the fate of a cell determined as Bcl-2 inhibits apoptosis?

A

-by the balance of activity of proapoptotic and antiapoptotic Bcl-2 family members

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17
Q

Bax and Bak

A
  • proapoptotic effector proteins
  • downstream effectors that directly induce apoptosis
  • inhibited by antiapoptotic Bcl-2
  • induce release of cytochrome c which triggers caspase activation
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18
Q

BH3-only members of Bcl-2 family

A
  • upstream

- when activated by cell death signals, they antagonize the Bcl-2 family and activate Bax and Bak

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19
Q

Caspase-9

A
  • key initiator caspase

- activated by forming a complex with Apaf-1 and cytochrome c in a complex called the apoptosome

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20
Q

Where is cytochrome c located in normal conditions?

A

-in the mitochondrial inter-membrane space

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21
Q

Where are Apaf-1 and caspase-9 located in normal conditions?

A

-in the cytosol

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22
Q

How are Intrinsic pathways to regulate cell death activated?

A

activated by DNA damage and other cell stress

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23
Q

How are Extrinsic pathways to regulate cell death activated?

A

activated by signals from other cells

24
Q

Transcription factor p53

A

-mediates a major pathway leading to cell cycle arrest in response to DNA damage

25
Q

How does p53 lead to cell death?

A
  • DNA damage leads to ATM and Chk2 protein kinase phosphorylation and stabilization of p53
  • results in rapid increase of p53 levels
  • p53 activates transcription of genes that encode the proapoptotic BH3-only proteins PUMA and NOXA which lead to cell dath
26
Q

proteins PUMA and Noxa

A
  • proapoptotic BH3-only proteins
  • lead to cell death
  • activated by p53
27
Q

PI 3-kinase

A
  • initiates a major signaling pathway that promotes cell survival.
  • phosphorylates PIP2 to form PIP3 which activates the protein-serine/threonine kinase Akt
28
Q

Akt

A
  • activated by PIP3
  • protein-serine/threonine kinase
  • phosphorylates a number of proteins that regulate apoptosis
29
Q

Extrinsic cell death pathway

A

a) signals are polypeptides in the TNF family
b) receptors activate an initator caspase: caspase 8
c) caspase 8 can cleave and/or activate effector caspases and Bid
d) Bid leads to acdivation of caspase 9

30
Q

Autophagy

A
  • programmed cell death by non-apoptotic mechanisms
  • a mechanism for gradual turnover of cell components in normal cells
  • in starvation conditions, degredation of components provides energy and recycles materials
  • autophagic cells don’t require caspases
31
Q

How are dying cells characterized?

A

by an accumulation of lysosomes

32
Q

when can autophagy be activated?

A

-by cellular stress and can provide an alternative to apoptosis when apoptosis is blocked

33
Q

What happens if differentiated cells in adult animals are lost?

A

-since most differentiated cells in adult animals are no longer capable of proliferation, if the cells are lost they are replace by proliferation of cells derived from self-renewing stem cells

34
Q

FIbroblasts

A
  • cells in connective tissue

- can proliferate quickly in response to platelet-derived growth factor (PDGF) released at the site of a wound

35
Q

Endothelial cells

A
  • line blood vessels and can proliferate to form new blood vessels for repair and regrowth of damaged tissue
  • proliferation triggered by vascular endothelial growth factor (VEGF) which is produced by cells that lack oxygen.
  • endothelial cells of some internal organs are able to proliferate to replace damaged tissue
36
Q

Liver cells

A
  • normally arrested in the G0 phase of the cell cycle.

- stimulated to priliferate if large numbers of liver cells are lost

37
Q

Stem cells

A
  • less differentiated
  • self-renewing cells
  • present in most adult tissues
  • retain capacity to proliferate and replace differentiated cells throughout the lifetime of an animal
  • stem cells will differentiate along specific pathways if appropriate growth factors are added
  • stem cells have been developed into neurons and used for transplantation
38
Q

Key properties of stem cells

A
  1. divide to produce one daughter cell that remains a stem cell and one daughter cell that divides and differentiates
  2. self renewing
  3. serve as a source of differentiated cells throughout life
39
Q

Give examples of cells that must continually be replaced

A

blood cells, sperm, epithelial cells of skin and in the lining of digestive track, cells of hair follicles and sebaceous glands

40
Q

Renewal of intestinal epithelium

A
  • epithelial cells that line the intestine only live a few days before they undergo apoptosis
  • new cells are derived from continuous and slow division of stem cells at the bottom of intestinal crypts
  • new cells proliferate for 3-4 cell divisions and then differentiate
41
Q

Satellite cells

A
  • stem cells of adult muscle

- normally arrested in G0, but they proliferate quickly in response to injury.

42
Q

Niches

A
  • distinct micro-environments where most adult tisssues have stem cells
  • provide the signals that maintain stem cells throughout life
  • control the balance between self-renewal and differentiation
43
Q

Hematopoietic stem cell transplantation

A

(bone marrow transplantation)

-important in treatment of many cancers to replace cells damaged by toxic chemotherapy drugs

44
Q

Epithelial stem cells

A

-used in the form of skin grafts to treat burns, wounds, and ulcers

45
Q

Epidermal skin cells

A
  • can be cultured and then transferred to the patient

- eliminates immune system rejection

46
Q

Embryonic stem cells

A
  • can be grown indefinetly as pure stem cell populations that have pluripotency
  • provide a model system to study events associated with cell differentitation
47
Q

pluripotency

A

the capacity to develop into all of the different types of cells in adult tissues

48
Q

Growth factor LIF

A
  • required to maintain cells in undifferentiated state

- if removed, cells aggregate and differentiate

49
Q

Somatic cell nuclear transfer

A
  • cloning
  • dolly the sheep
  • inserting nucleus of adult somatic cell into enucleated egg, allowing it to culture
50
Q

Therapeutic cloning

A

-a nucleus from an adult human cell would be transferred to an enucleated agg, the resulting embryo could produce differentiated cells for transplatation therappy, this would bypass the problem of tissue rejection

51
Q

Therapeutic cloning: problems to overcome

A

a) low efficiency of generating embryos by somatic cell nuclear transfer
b) ethical concerns with respect to cloning of human beings (reproductive cloning with respect to destruction of embryos

52
Q

How can induced pluripotent stem cells overcome problems of therapeutic cloning?

A
  • reprogramming somatic cells to resemble embryonic stem cells
  • adult human fibroblasts can be reprogrammed to pluripotency
53
Q

Induced pluripotent stem cell technique

A

-infect an adult mouse fibroblast with a retrovirus carrying genes for Oct 4, Sox2, Klf4, and c-Myc transcription factors

54
Q

Transcription factors that play a central role in inducing pluripotency?

A

Oct 4, Sox2, Nanog

  • factors form an auroregulatory loop, positively regulating each others expression
  • activate other genes that maintain the pluripotent state, while repressing genes that enable differentiation
55
Q

Transdifferentiation

A

Reprogramming somatic cells to other types of differentiated cells
-would bypass need for pluripotent stem cells
(mouse fibroblasts have been turned into heart muscle and nerve cells using only three transcription factors)

Molecular Cell Biology (16 decks)

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