Apoptosis is a programmed cell death process that occurs normally during development and aging and as a defense mechanism. There are two main pathways of apoptosis - the intrinsic mitochondrial pathway initiated from within the cell, and the extrinsic death receptor pathway initiated from outside the cell. Both pathways involve caspase proteins that activate a caspase cascade leading to characteristic cell changes and death. Apoptosis must be tightly regulated as both insufficient and excessive apoptosis can lead to disorders.

1. G.D. RUNGTA COLLEGE OF SCIENCE & TECHNOLOGY
KOHKA-KURUD,BHILAI ,DURG(C.G.)
A
SEMINAR ON
APOPTOSIS
GUIDED BY:
MISS SUMAIYA ARSHI
PRESENTED BY:
LATA GULBAKE
MSC1ST SEM
BIOTECHNOLOGY

2. Index
1. Introduction
2. Cell death
3. The caspase family
4. Intrinsic pathway
5. Extrinsic pathway
6. Need of apoptosis
7. Disorders
8. Conclusion
9. Bibliography

3. Introduction
• Apoptosis is the process of programmed cell death.
• Apoptosis occurs normally during development and aging and as a
homeostatic mechanism to maintain cell populations in tissues.
• Apoptosis also occurs as a defense mechanism such as in immune
reactions or when cells are damaged by disease or noxious agents.
• Biochemical events lead to characteristic cell changes (morphology) and
death. These changes include blebbing, cell shrinkage, nuclear
fragmentation, chromatin condensation, and chromosomal DNA
fragmentation.
• German scientist Carl Vogt was first to describe the principle of apoptosis in
1842.
Cell Death
• Cell die by one of two mechanisms-
• Necrosis - Death By Injury
• Apoptosis - Death By Suicide

4. The Caspase Family
• Caspases or cysteine-aspartic proteases or cysteine dependent aspartate-directed proteases are
a family of cysteine proteases that play essential roles in apoptosis (programmed cell death),
necrosis, and inflammation.
• Single chain of pro-enzymes.
3 Types of Caspases
• Inflammatory Caspases: 1, 4, and 5
• Initiator Caspases: 2, 8, 9, and 10
• Effector Caspases: 3, 6, and 7

5. Intrinsic pathway or mitochondrial pathway
• Initiated from within the cell.
• In the intrinsic pathway mitochondria become leaky and ooze out of
proteins called cytochrome C, which initiate apoptosis usually the
cytoplasm and mitochondrial membrane harbour proteins called Bcl-2 and
Bcl-X which are anti-apoptotic and presence the integrity of the
mitochondrial membrane preventing apoptotic proteins like cytochrome C
from leaking into the cytoplasm.
• However, in the absence of a growth signal or insult due to radiation or
protein misfolding.Stress proteins called “BH3 only” proteins are
stimulated.
• “BH3 only” proteins comprising of Bim, Bid and Bad proteins block the
function of Bcl-2 and Bcl-X.
• These proteins further activate two pro-apoptotic effectors called Bax and
Bak, which create channels in the mitochondrial membrane, allowing intra-
mitochondrial proteins like cytochromeC to leak into the cytoplasm.
• CytochromeC, in the cytoplasm binds with a protein called Apaf-1
(Apoptosis activating factor 1) to form a complex called apoptosome.
• This complex binds with caspase 9 and begins to cleave and activate
adjacent caspase 9 molecules activate executioner caspases like 3 and 7
leading to apoptosis of the cell.

6. Extrinsic pathway or Death receptor pathway
• Begins outside the cells.
• The extrinsic pathway involves binding of an adapter protein called
Fas-associated death domain (FADD) to the cytoplasmic end of
atleast 3-4 Fas ligands.
• This then binds with caspase 8, an initiator caspase, which gets
cleaved to become active.
• The active caspase 8 further activates other caspase 8 molecules.
• This in turn activate executioner caspase 3 and 7 leading to
apoptosis of the cell.

7. Execution of Apoptosis
• Executioner caspase 3 and 7 cause
degradation of chromosomal DNA and also
degradation of cytoskeletal proteins, which
cause the morphological changes such as
nuclear fragmentation and cellular shrinkage
respectively.
• Apoptotic bodies are coated with a
phospholipid called phosphatidylserine which
is recognized by phagocyte receptors.

8. Apoptosis: Pathways
“Extrinsic pathway”
Death
Ligands
Death
Receptors
Initiator
Caspase 8
Effector
Caspase 3
DNA damage
& P53
Mitochondrial/
Cytochrome C
Initiator
Caspase 9
Cell Death
“Intrinsic pathway”

9. • Apoptosis is needed for proper development, Examples:
• The resorption of the tadpole tail
• The formation of the fingers and toes of the fetus
• The formation of the proper connections between neurons in the brain
• Apoptosis is needed to destroy cells, Examples:
• Cells infected with viruses
• Cells with DNA damage
• Cancer cells
Disorders
1. Disorders where apoptosis is inhibited (decreased apoptosis,increase in cell survival)
• Cancer
• Autoimmune disorder
• Viral infections
2. Disorders where apoptosis is excessive increase in cell death (Means hyperactive apoptosis)
• AIDS
• Neurodenegrative disorder
Need Of Apoptosis

10. Conclusion
• Apoptosis is a multifunctional defense system which protects the host's body from infectious, genetical and
immunological diseases and disorders. Simultaneously, apoptosis mediates an enzymatic cascade system
which plays a vital role in the process of apoptosis. The presence or absence, the rate and concentration of
each enzyme reveal the situation of the body and determine the type of diseases. Thus, the study of the type
and concentration of the caspase enzymes is valuable criterion for diagnosing and treatment.
Bibliography
• Molecular Biology of the Cell (6th edition)
• Gerald karp – cell and microbiology (5th edition)
• Cell and molecular biology and genetics by Dr. N. Arumugam