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Presented by
Biswajit Sahoo
Ph.D. 1st year
 Cells committing suicide by the activation of an
intracellular death program.
 Apoptosis (APP-oh-TOE-sis, John Kerr et al. 1972) means
Falling Off, like the leaves of a tree in autumn.
 A neat, silent death of cells.
 No damage to neighboring cells, as in Necrosis - Cell
death by swelling and exploding due to injury or damage.
 Different from autophagy – intracellular digestion by acid
hydrolases of Lysosomes.
 Mainly mediated by a group of proteolytic
enzymes called Caspases.
 Present in all cells in an inactive form called
Pro- Caspases.
 Activated to kill cells by death signals.
 The Poison Pills of Cells.
 Reception of death or apoptotic signals (Internal /
external).
 Activation of Inactive Procaspases to active Caspases
(Cascade Reaction).
 Degradation of cytoplasmic and nuclear proteins.
 Fragmentation of DNA/Nucleus.
 Shrinkage and blebbing of cells.
 Formation of smaller membrane bound structures called
apoptotic bodies.
 Digestion of apoptotic bodies by macrophages –
Phagocytosis.
 Recycling of the macro-molecules.
A normal cell An apoptotic cell
A normal cell
 Normal process during development.
 Responsible for formation of body parts during development of
animals.
 Development of animal palm.
 Metamorphosis of tadpole into Frog, insect larva into pupa.
 Eliminating unwanted / improperly formed / functionless / dangerous
cells.
 Virus infected cells, cancer cells, improperly developed thymocytes,
activated lymphocytes.
 Killing cancer cells by activating PCD.
 Certain auto-immune diseases are due to failure of apoptosis in cells
which should die.
 Apoptosis in cells which should not die leads to abnormal development
/ disorders (Neuro– degenerative problems).
 Degradation of Nucleus.
 Disappearance of cytoplasm.
 Packaging inside small vacuoles.
 Apoptosis is an integral part of plant
ontogenesis; it is controlled by cellular
oxidative status, phytohormones, and DNA
methylation.
 In wheat plants apoptosis appears at early
stages of development in coleoptile and initial
leaf of 5-6 days old seedlings.
 Peroxides, abscisic acid, ethylene releaser ethrel, and DNA
methylation inhibitor 5-azacytidine induce and stimulate
apoptosis.
 Modulation of the reactive oxygen species (ROS) level in
seedling by antioxidants and peroxides results in tissue-specific
changes in the target date for the appearance and the
intensity of apoptosis.
 Antioxidant butylated hydroxytoluene (BHT) reduces the
amount of ROS and prevents apoptosis in etiolated seedlings,
prolongs coleoptile life span, and prevents the appearance of
all apoptotic features mentioned.
 In roots of etiolated wheat seedlings, BHT induces
differentiation of plastids with the formation of
chloro(chromo)plasts.
 Therefore, ROS controlled by BHT seems to regulate mitosis,
trigger apoptosis, and control plastid differentiation and the
organization of various cellular structures formed by
endocytoplasmic reticulum.
 During pollination, plants enforce self-incompatibility (SI)
as an important means to prevent self-fertilization.
 Research on the corn poppy (Papaver rhoeas) has
revealed that proteins in the pistil on which the pollen
lands, interact with pollen and trigger PCD in incompatible
(i.e., self) pollen.
 The researchers, Steven G. Thomas and Veronica E.
Franklin- Tong, also found that the response involves rapid
inhibition of pollen-tube growth, followed by PCD.
Nucleus and cytoplasm degraded by apoptosis
Apoptotic vacuoles with cellular debris
Cells get injured, cells get punctured where cells lyse extruding various
Injurious components, which cause severe damage to other
neighboring cells, causing a widespread destruction; this is like carnage.
Apoptosis
Apoptosis
Apoptosis

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Apoptosis

  • 2.  Cells committing suicide by the activation of an intracellular death program.  Apoptosis (APP-oh-TOE-sis, John Kerr et al. 1972) means Falling Off, like the leaves of a tree in autumn.  A neat, silent death of cells.  No damage to neighboring cells, as in Necrosis - Cell death by swelling and exploding due to injury or damage.  Different from autophagy – intracellular digestion by acid hydrolases of Lysosomes.
  • 3.  Mainly mediated by a group of proteolytic enzymes called Caspases.  Present in all cells in an inactive form called Pro- Caspases.  Activated to kill cells by death signals.  The Poison Pills of Cells.
  • 4.  Reception of death or apoptotic signals (Internal / external).  Activation of Inactive Procaspases to active Caspases (Cascade Reaction).  Degradation of cytoplasmic and nuclear proteins.  Fragmentation of DNA/Nucleus.  Shrinkage and blebbing of cells.  Formation of smaller membrane bound structures called apoptotic bodies.  Digestion of apoptotic bodies by macrophages – Phagocytosis.  Recycling of the macro-molecules.
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  • 6. A normal cell An apoptotic cell A normal cell
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  • 13.  Normal process during development.  Responsible for formation of body parts during development of animals.  Development of animal palm.  Metamorphosis of tadpole into Frog, insect larva into pupa.  Eliminating unwanted / improperly formed / functionless / dangerous cells.  Virus infected cells, cancer cells, improperly developed thymocytes, activated lymphocytes.  Killing cancer cells by activating PCD.  Certain auto-immune diseases are due to failure of apoptosis in cells which should die.  Apoptosis in cells which should not die leads to abnormal development / disorders (Neuro– degenerative problems).
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  • 18.  Degradation of Nucleus.  Disappearance of cytoplasm.  Packaging inside small vacuoles.  Apoptosis is an integral part of plant ontogenesis; it is controlled by cellular oxidative status, phytohormones, and DNA methylation.  In wheat plants apoptosis appears at early stages of development in coleoptile and initial leaf of 5-6 days old seedlings.
  • 19.  Peroxides, abscisic acid, ethylene releaser ethrel, and DNA methylation inhibitor 5-azacytidine induce and stimulate apoptosis.  Modulation of the reactive oxygen species (ROS) level in seedling by antioxidants and peroxides results in tissue-specific changes in the target date for the appearance and the intensity of apoptosis.  Antioxidant butylated hydroxytoluene (BHT) reduces the amount of ROS and prevents apoptosis in etiolated seedlings, prolongs coleoptile life span, and prevents the appearance of all apoptotic features mentioned.  In roots of etiolated wheat seedlings, BHT induces differentiation of plastids with the formation of chloro(chromo)plasts.  Therefore, ROS controlled by BHT seems to regulate mitosis, trigger apoptosis, and control plastid differentiation and the organization of various cellular structures formed by endocytoplasmic reticulum.
  • 20.  During pollination, plants enforce self-incompatibility (SI) as an important means to prevent self-fertilization.  Research on the corn poppy (Papaver rhoeas) has revealed that proteins in the pistil on which the pollen lands, interact with pollen and trigger PCD in incompatible (i.e., self) pollen.  The researchers, Steven G. Thomas and Veronica E. Franklin- Tong, also found that the response involves rapid inhibition of pollen-tube growth, followed by PCD.
  • 21. Nucleus and cytoplasm degraded by apoptosis
  • 22. Apoptotic vacuoles with cellular debris
  • 23. Cells get injured, cells get punctured where cells lyse extruding various Injurious components, which cause severe damage to other neighboring cells, causing a widespread destruction; this is like carnage.