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By- Nisha Lakra
M.Sc 2nd SEMESTER
DEPARTMENT OF Applied genetics
Brindavan College
 Apoptosis is the process of programmed cell
death.
 The word apoptosis was introduced by Kerr,
Wyllie and Currie to describe a form of cell death
distinct from necrosis.
Apoptosis
• Chromatin condensation
• Cell Shrinkage
• Preservation of
Organelles
and cell membranes
• Rapid engulfment by
neighboring cells
preventing inflammation
Necrosis
• Nuclear swelling
• Cell Swelling
• Disruption of Organelles
• Rupture of cell and
release
of cellular contents
• Inflammatory response
Apoptosis is an energy dependent programmed
cell death for removal of unwanted individual
cells
Death
Ligands
Effector
Caspase 3
Death
Receptors
Initiator
Caspase 8
Cell
death
DNA
damage
& p53
Mitochondria/
Cytochrome C
Initiator
Caspase 9
“Extrinsic Pathway”
“Intrinsic Pathway”
• They belong to a group of enzymes known as cysteine
proteases,Zymogens- inactive forms.
• Caspase 8 and 10- initiator (extrinsic)
• Caspase 9- initiator (intrinsic)
 Single chain of pro-enzymes.
 Contains an N-terminal domain, a small subunit and
a large subunit (similar to a ribosome).
 Apoptotic stimulus Activation Substrate
Cleavage Enzyme.
 Inflammatory Caspases: 1, 4, and 5
 Initiator Caspases: 2, 8, 9, and 10
 Long N-terminal domain
 Interact with effector caspases
 Effector Caspases: 3, 6, and 7
 Little to no N-terminal domain
 Initiate cell death
 It involves transmembrane death receptors that are
members of the tumor necrosis factor (TNF) receptor
gene superfamily.
 ligands of these receptors are FasL, TNF-alpha,
Apo3L, and Apo2L. Corresponding receptors are FasR,
TNFR1, DR3, and DR4/DR5, respectively.
 The signal transduction of the extrinsic pathway
involves several caspases which are proteases with
specific cellular targets.
 It involves non-receptor–mediated
intracellular signals, inducing activities in
the mitochondria that initiate apoptosis.
 Pro-apoptotic proteins activate caspases
that mediate the destruction of the cell
through many pathways.
 The regulation of pro-apoptotic events in
the mitochondria occurs through activity
of members of the Bcl-2 family of proteins
and the tumor suppressor protein p53.
 Members of the Bcl-2 family of proteins
may be pro- or anti-apoptotic.
 The anti-apoptotic proteins are Bcl-2, Bcl-
x, Bcl-xL, Bcl-XS, Bcl-w, and BAG.
 Pro-apoptotic proteins include Bcl-10,
Bax, Bak, Bid, Bad, Bim, Bik, and Blk.
Mechanism (Intrinsic)
IMPORTANCE OF APOPTOSIS
o Important in normal physiology / development
– Development: Immune systems maturation,
Morphogenesis, Neural development
– Adult: Immune privilege, DNA damage and wound
repair.
o Excess apoptosis
– Neurodegenerative diseases
o Deficient apoptosis
– Cancer
– Autoimmunity
APOPTOSIS: important in embryogenesis
Morphogenesis (eliminates excess cells):
Selection (eliminates non-functional cells):
APOPTOSIS: important in embryogenesis
Immunity (eliminates dangerous cells):
Self antigen
recognizing cell
Organ size (eliminates excess cells):
Thank you

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Apoptosis

  • 1. By- Nisha Lakra M.Sc 2nd SEMESTER DEPARTMENT OF Applied genetics Brindavan College
  • 2.  Apoptosis is the process of programmed cell death.  The word apoptosis was introduced by Kerr, Wyllie and Currie to describe a form of cell death distinct from necrosis.
  • 3. Apoptosis • Chromatin condensation • Cell Shrinkage • Preservation of Organelles and cell membranes • Rapid engulfment by neighboring cells preventing inflammation Necrosis • Nuclear swelling • Cell Swelling • Disruption of Organelles • Rupture of cell and release of cellular contents • Inflammatory response
  • 4. Apoptosis is an energy dependent programmed cell death for removal of unwanted individual cells
  • 5. Death Ligands Effector Caspase 3 Death Receptors Initiator Caspase 8 Cell death DNA damage & p53 Mitochondria/ Cytochrome C Initiator Caspase 9 “Extrinsic Pathway” “Intrinsic Pathway”
  • 6. • They belong to a group of enzymes known as cysteine proteases,Zymogens- inactive forms. • Caspase 8 and 10- initiator (extrinsic) • Caspase 9- initiator (intrinsic)  Single chain of pro-enzymes.  Contains an N-terminal domain, a small subunit and a large subunit (similar to a ribosome).  Apoptotic stimulus Activation Substrate Cleavage Enzyme.
  • 7.  Inflammatory Caspases: 1, 4, and 5  Initiator Caspases: 2, 8, 9, and 10  Long N-terminal domain  Interact with effector caspases  Effector Caspases: 3, 6, and 7  Little to no N-terminal domain  Initiate cell death
  • 8.  It involves transmembrane death receptors that are members of the tumor necrosis factor (TNF) receptor gene superfamily.  ligands of these receptors are FasL, TNF-alpha, Apo3L, and Apo2L. Corresponding receptors are FasR, TNFR1, DR3, and DR4/DR5, respectively.  The signal transduction of the extrinsic pathway involves several caspases which are proteases with specific cellular targets.
  • 9.
  • 10.  It involves non-receptor–mediated intracellular signals, inducing activities in the mitochondria that initiate apoptosis.  Pro-apoptotic proteins activate caspases that mediate the destruction of the cell through many pathways.  The regulation of pro-apoptotic events in the mitochondria occurs through activity of members of the Bcl-2 family of proteins and the tumor suppressor protein p53.  Members of the Bcl-2 family of proteins may be pro- or anti-apoptotic.  The anti-apoptotic proteins are Bcl-2, Bcl- x, Bcl-xL, Bcl-XS, Bcl-w, and BAG.  Pro-apoptotic proteins include Bcl-10, Bax, Bak, Bid, Bad, Bim, Bik, and Blk.
  • 12. IMPORTANCE OF APOPTOSIS o Important in normal physiology / development – Development: Immune systems maturation, Morphogenesis, Neural development – Adult: Immune privilege, DNA damage and wound repair. o Excess apoptosis – Neurodegenerative diseases o Deficient apoptosis – Cancer – Autoimmunity
  • 13. APOPTOSIS: important in embryogenesis Morphogenesis (eliminates excess cells): Selection (eliminates non-functional cells):
  • 14. APOPTOSIS: important in embryogenesis Immunity (eliminates dangerous cells): Self antigen recognizing cell Organ size (eliminates excess cells):