NISHA SALAME CELL DEATH for Nsc Students.pdf

A brief description about cell death.

1. CELL DEATH
SESSION – (2023-2024SESSION – (2023-2024)SESSION – (2023-2024SESSION – (2023-2024)



GOVGOVGOVTTT. V.Y.T. PG . V.Y.T. PG . V.Y.T. PG AUTONOMOUS AUTONOMOUS AUTONOMOUS GOVT. V.Y.T. PG AUTONOMOUS GOVT. V.Y.T. PG AUTONOMOUS GOVT. V.Y.T. PG AUTONOMOUS
COLLEGE, DURGCOLLEGE, DURGCOLLEGE, DURGCOLLEGE, DURGCOLLEGE, DURGCOLLEGE, DURG
DEPARTMENT OF BIOTECHNOLOGY
PRSENTATION ONPRSENTATION ONPRSENTATION ONPRSENTATION ON



GUIDED BY:-GUIDED BY:-
DR. SHWETA PANDEYDR. SHWETA PANDEY

SUBMITTED BY:-SUBMITTED BY:-
NISHA SALAMENISHA SALAME
M.Sc. 1
st
SEMM.Sc. 1
st
SEM

2. SYNOPSIS OF CELL DEATHSYNOPSIS OF CELL DEATH
1.
2.
3.
4.
5.
6.
7.
8.
9.
What is cell death ? ( Intro)What is cell death ? ( Intro)
Why it happens ?Why it happens ?
Types of cell deathTypes of cell death
Difference between necrosis & apoptosisDifference between necrosis & apoptosis
Mechanisms Mechanisms
PathwaysPathways
ImportanceImportance
ConclusionConclusion
ReferenceReference

3. INTRODUCTIONINTRODUCTION
The cell undergoes a natural
process of death after
completing a number of cell
divisions.
The cell undergoes a natural
process of death after
completing a number of cell
divisions.
The cell ceases to carry out its
functions and dies to be
replaced by new ones.
The cell ceases to carry out its
functions and dies to be
replaced by new ones.

4. WHY IT
HAPPENES
If cells are no longer needed they
commit suicide by activating an
intracellular death program.
If cells are no longer needed they
commit suicide by activating an
intracellular death program.

5. TYPES OF CELL
DEATH
TYPES OF CELL
DEATH
Cells that die as a
result of a acute
external injury
typically swell and
burst.
Cells that die as a
result of a acute
external injury
typically swell and
burst.
APOPTOSISAPOPTOSISNECROSIS NECROSIS
Cell death by signaling Cell death by signaling
/programmed cell death/programmed cell death
it is used during earlyit is used during early
development to eliminatedevelopment to eliminate
unwanted cells.unwanted cells.

6. 1.
2.
3.
Cell death byCell death by
injury/exposure to toxicinjury/exposure to toxic
chemicalchemical
Cell death by
injury/exposure to toxic
chemical.
Cell death by
injury/exposure to toxic
chemical.

Cell Swell & Burst Cell Swell & Burst Cell Swell & Burst Cell Swell & Burst
plasma plasma plasma plasma
membrane membrane membrane membrane
lyses. lyses. lyses. lyses.

Cell constant spill out Cell constant spill out Cell constant spill out Cell constant spill out
and effect neighbouring and effect neighbouring and effect neighbouring and effect neighbouring
cells also cells also cells also. cells also.

These causes These causes 4. These causes 4. These causes
inflammatory inflammatory inflammatory inflammatory
reaction. reaction. reaction. reaction.
1.
2.
It is a programmed cell death inIt is a programmed cell death in
multicellular organism.multicellular organism.
It is a programmed cell death in
multicellular organism.
It is a programmed cell death in
multicellular organism.

Cell Shrinkage of Cell Shrinkage of Cell Shrinkage of Cell Shrinkage of
cytoplasm and cytoplasm and cytoplasm and cytoplasm and
permanent nucleus permanent nucleus permanent nucleus permanent nucleus
condensation condensation condensation. condensation.

Segmentation of chromatin Segmentation of chromatin 3. Segmentation of chromatin 3. Segmentation of chromatin
and formation of bleb and formation of bleb and formation of bleb. and formation of bleb.

Cell undergoes to Cell undergoes to 4. Cell undergoes to 4. Cell undergoes to
phagocytosis phagocytosis.. phagocytosis. phagocytosis.
NECROSISNECROSIS APOPTOSISAPOPTOSIS

7. APOPTOSIS
APOPTOSIS
MORPHOLOGICALMORPHOLOGICAL
CHANGES:-CHANGES:-
(comes) from greek word meaning
Cell shrinkage
Chromatin condensation
DNA fragmentation
mRNA decay
Blebbing
Lysis
'falling off'

8. These electron micrographs show cells that have died by (A) necrosis or (B and C) apoptosis. The cells in (A) and (B) died in a
culture dish, whereas the cell in (C) died in a developing tissue and has been engulfed by a neighboring cell. Note that the cell in (A)
seems to have exploded, whereas those in (B) and (C) have condensed but seem relatively intact. The large vacuoles visible in the
cytoplasm of the cell in (B) are a variable feature of apoptosis.

9. MECHANISM
The Intracellular machinery are responsible for apoptosisThe Intracellular machinery are responsible for apoptosis.
Machinery depends on a family of proteases called
caspases
Machinery depends on a family of proteases called
caspases.
They have a cysteine at their 'active site' & and cleave
their target specific aspartic acids.
They have a cysteine at their 'active site' & and cleave
their target specific aspartic acids.
# Apoptosis is mediated by an Intracellular Proteolytic Cascade:-# Apoptosis is mediated by an Intracellular Proteolytic Cascade:-
Cysteine Aspartic

11. 1.
Capase are synthesized in
the cell as inactive form of
Capase are synthesized in
the cell as inactive form of
procaspaseprocaspase.
MECHANISM
These procaspases are activate by
cleavage at aspartic acids by other
caspase.
These procaspases are activate by
cleavage at aspartic acids by other
caspase.
2.
Once its activated they cleave
and there by activate other
procaspases resulting in an
amplifying proteolytic cascade.
Once its activated they cleave
and there by activate other
procaspases resulting in an
amplifying proteolytic cascade.
3.
They have ability to degrade
target cell proteins and some
caspase are nuclease that
degrades DNA.
They have ability to degrade
target cell proteins and some
caspase are nuclease that
degrades DNA.
4.
The protease cascade is not
only destructive and self
amplifying but also irreversible.
The protease cascade is not
only destructive and self
amplifying but also irreversible.
5.

12. 2 TYPES OF PATHWAY 2 TYPES OF PATHWAY
EXTRINSIC
PATHWAY
Procaspase activation
can be triggered from
outside the cell by
activation of death
receptor on the cell
surface.
1.
INTRINSIC PATHWAY
Procaspase
activation can be
initiate under cell.
2.

13. EXTRINSIC PATHWAY

14. EXTRINSIC PATHWAY
oFas protein binds with intracellular "adaptor proteins" that aggregate
with procaspase 8 molecule and make complex.
oKiiler Lymphocyte producing a protein called Fas ligand.
Then caspase 8 molecule is activated by cleave one another and they
are activate other downstream procaspase and induce apoptosis.
Fas ligand binds with Fas protein of death receptor on the surface
of target cell.
By extracellular stimuliBy extracellular stimuli

15. INTRINSIC PATHWAY

16. INTRINSIC PATHWAY
oWhen cells are damaged or stressed they can also kill themselves by
triggering procaspase activation from within the cell.
oEg. If mitochondria are injured they are induced to release the
electron carrier protein cytochrome c into cytosol.
By extracellular stimuliBy extracellular stimuli
oWhere its bind and activate adaptor protein called Apaf – 1.
oAggregation of Apaf 1 and binding of 'procaspase – 9'.
oActivation of procaspase – 9 and make Caspase Cascade.
oApoptosis.

17. These protein belongs to Bcl-2 protein family.
This response usually require p53 protein which can
recognize damaged - DNA and activates the
transcriptions of genes that encode proteins that
promote the release of cytochrome – 6 from
mitochondria.

18. •Bcl-2 family Bcl-2 family
Some members of this familySome members of this family
Bcl-2 itself Bcl-2 itself
Main Intracellular Regulator of Cell Death Program
•IAP IAP
Bcl-XlBcl-Xl
Inhibit apoptosis by blocking the release of cytochrome
c from mitochondria.
APOPTOSIS INHIBITING MEMBER
●BaxBax
●BakBak
Promote procaspase activation and cell death stimulate the
release of cytochrome c
APOPTOSIS PROMOTING MEMBER
If the gene encoding Bax and Bak are both inactivated cells are remarkably
resistant to most apoptosis inducing stimuli.
If the gene encoding Bax and Bak are both inactivated cells are remarkably
resistant to most apoptosis inducing stimuli.

19. INHIBITOR OF APOPTOSIS
1.They bind to some procaspase to prevent their
activation.

2. They bind to caspase to inhibit their activity.
These proteins are inhibit apoptosis in two ways:-
(IAP family)

20. IMPORTANCE
Cell death balances the cell division.
(A) The paw in this mouse embryo has been stained
with a dye that specifically labels cells that have
undergone apoptosis. The apoptotic cells appear
as bright green dots between the developing digits.
(B) This interdigital cell death eliminates the
tissue between the developing digits, as seen one
day later, when few, if any, apoptotic cells can be
seen.
As a tadpole changes into a frog, the cells in the
tadpole tail are induced to undergo apoptosis; as a
consequence, the tail is lost. All the changes that
occur during metamorphosis, including the induction
of apoptosis in the tail, are stimulated by an
increase in thyroid hormone in the blood.

21. CONCLUSIONS



Apoptosis is a form of programmed cell death, or "cellular suicide" (different from
necrosis, in which cells die due to injury).

Apoptosis is an orderly process in which the cell's contents break down and are
packaged into small packets of membrane for "garbage collection" by immune cells
(contrasting with necrosis in which the dying cell's contents spill out and cause
inflammation).

Apoptosis removes cells during development. It also eliminates pre-cancerous and virus
-infected cells. Apoptosis maintains the balance of cells in the human body and is
particularly important in the immune system.

22. REFERENCE
The Cell
- Cooper
https://www.ncbi.nlm.nih.gov/book