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Lecture 17

MCD BIO 165A Lecture 17: lecture 17 apoptosisPremium

10 pages66 viewsFall 2018

Department
Molecular, Cell, and Developmental Biology
Course Code
MCD BIO 165A
Professor
arispe
Lecture
17

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Lecture 17
ATP continued & Apoptosis
ATP formation machinery
H+ gradient drives transport of ADP into and
ATP out of the mitochondria
ADP as most important factor controlling
respiration rate
Mitochondria-related Diseases
Prematured-aging phenotype caused by
increased mutation in mtDNA.
- Defective nuclear gene encodes for DNA
polymerase responsible for mtDNA
replication
Speculation: accumulation of mutations in
mtDNA as major cause of aging
Additional findings: mtDNA mutation may
cause premature aging but not sufficient for
normal aging process
Apoptosis
Apoptotic cells have blebbing membrane
Cell death
- By Injurious agents necrosis
- By program cell death apoptosis
B cells in neck lymph nodes make antibodies; when activated, they differentiate like crazy
(lymph nodes swelling)
- When no longer ill, most of those B cells die in order to ensure that we can efficiently
cope with same bacteria again
Apoptosis & necrosis
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Necrosis
- When a heart vessel blocked, cardiomyocytes can’t get O2 -> mitochondria & cell
swell -> plasma membrane rupture -> cell content leaks to extracellular space,
including lysosomal enzyme
- If lots of cells do necrosis at the same time -> pH lowers significantly -> massive tissue
destruction -> heart attack/stroke
- Can have extensive tissue damage (cell spilling its guts!) depending on number of cell
affected
Apoptosis
- Program cell death
- Cell dehydration while membrane maintains integrity -> cell shrinks & content
digestion, chromatin condensation, contained within the cell so that membrane
retains all enzymes executing the process
- Apoptotic cells phagocytosed by macrophages prior to releasing contents
- NO tissue damage or inflammation, only apoptotic cell affected
Apoptosis
Ordered process involving cell shrinkage, loss of adhesion to other cells, dissection of
chromatin & engulfment by phagocytosis
“death by suicide”
- Cell shrinkage
- Mitochondria breaking down -> releases cytochrome c
- Develop bubble-like blebs on membrane
- Chromatin degrades in nucleus
- Break into small, membrane-wrapped fragments which are usually engulfed by
phagocytic cells e.g. macrophages
When?
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- During embryonic development to form structures
E.g. formation of digits/fingers (carving out structure)
E.g. formation of CNS: neurons that don’t have proper terminal contact with
target do apoptosis
- Also active in adult
- Abnormal apoptosis linked to diseases e.g. cancer, Parkinson’s, Alzheimer’s,
Huntington’s diseases, Diabetes type I
Prevailing Cancer: cells regulating apoptosis affected
Targets
- Cells infected with viruses
- Cells of immune system
- Cells with DNA damage
- Cancer cells
How come?
- Survival signals: growth factors, integrins etc depending on different cells
- Negative singals: death activators, DNA-damaging agents, reactive Oxygen species,
etc
Mitochondria need cytochrome c to stay in inner membrane! Any stimulation
disturbs mitochondria membrane integrity & lets cytochrome c out triggers
apoptosis
- Survival vs negative signals
- Cells can repair some DNA damage, but only to an extent; beyond that -> apoptosis
- Signal triggering apoptosis
Increased level of oxidants in cell
Damage of DNA e.g. UV, X-ray, chemotherapeutic drugs (intrinsic)
Molecules binding to specific receptors on cell surface & signal the cell to begin
apoptotic cascade, e.g. TNF, lymphotoxin, fas Ligand
Mechanisms
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