Transcript Plant PCD In vegetative development Suspensor degradation

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Plant Biology 13:66
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Male Sterile and Maintainer Lines in Capsicum annuum L.(2013) Int.
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Aging
Genome
1. DNA damage
2. Epigenetic shifts
3. Telomere shortening
Cellular level
1. Mitochondria: ROS, DNA damage, other
2. Misfolded proteins
3. Dysfunctional stem cells
Organismal level
1. Autoimmune, other defects in immune system
2. Defective signaling
Apoptosis
Two basic steps: commitment and execution
Commitment depends on interplay between various signals
Bax & Bcl2 have opposite effects
2 main pathways: extrinsic & intrinsic
Procaspase 8 binds FADD
Procaspase 8 is processed to caspase 8
= initiator caspase
Caspase 8 converts procaspase 3
to active form = executioner
Caspase-3 & CAD
execute the cell
Intrinsic pathway
Usually Bcl-2 protects mito
Intracellular damage activates Bad or Bax
Apoptosis
Usually Bcl-2 protects mito
Intracellular damage activates Bad or Bax
Bad/Bax releases cyt c & AIF
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
Cyt c, Apaf-1 & procaspase-9 form
complex = apoptosome
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome
Apoptosome processes procaspase -9 to caspase-9 = initiator caspase
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome
Apoptosome processes procaspase -9 to caspase-9 = initiator caspase
Caspase-9 converts
caspase 3 to active
form = executioner
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
Cyt c, Apaf-1 & procaspase-9 form complex = apoptosome
Apoptosome processes procaspase -9 to caspase-9 = initiator caspase
Caspase-9 converts
caspase 3 to active
form = executioner
Caspase 3 & CAD
execute the cell
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
AIF induces CAD
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
AIF induces CAD
Destroys DNA
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
AIF induces CAD
Destroys DNA
Flips PS outside
Apoptosis
Intracellular damage activates Bad/Bax
Bad/Bax release cyt c & AIF
AIF induces CAD
Destroys DNA
Flips PS outside
Phagocytic cells eat
vesicles with
external PS
Apoptosis
Two basic steps: commitment and execution
Commitment depends on interplay between various signals
TNF often stimulates recovery instead!
Apoptosis in immunity
PD1 receptor on T cells blocks apoptosis
Binds PDL1 or PDL2 presented by other cells, including tumors
Apoptosis in immunity
PD1 receptor on T cells blocks apoptosis
Binds PDL1 or PDL2 presented by other cells, including tumors
PDL1 inhibitors are a new class of cancer drug
Autophagy
•Intracellular recycling process – lysosomes (animals);
vacuoles (plants)
Autophagy
•Intracellular recycling process – lysosomes (animals);
vacuoles (plants)
•Removes misfolded proteins, bad organelles, intracell pathogens
Autophagy
•Intracellular recycling process – lysosomes (animals);
vacuoles (plants)
•Removes misfolded proteins, bad organelles, intracell pathogens
•Promotes survival!
Autophagy
•Intracellular recycling process – lysosomes (animals);
vacuoles (plants)
•Removes misfolded proteins, bad organelles, intracell pathogens
•Promotes survival! Reallocates nutrients to vital processes!
Autophagy
• Removes misfolded proteins, bad organelles, intracell pathogens
• Promotes survival! Reallocates nutrients to vital processes!
• Best way to get rid of bad mito w/o killing cell!
•
•
•
•
Autophagy
Removes misfolded proteins, bad organelles, intracell pathogens
Promotes survival! Reallocates nutrients to vital processes!
Best way to get rid of bad mito w/o killing cell!
Associated with increased longevity in caloric restriction
Autophagy
• Associated with increased longevity in caloric restriction
• Upregulated upon nutrient or growth factor deprivation
Autophagy
•Associated with increased longevity in caloric restriction
•Upregulated upon nutrient or growth factor deprivation
•Triggers PCD distinct from apoptosis if can’t cope
• No caspase or CAD, chromatin laddering
• Occurs inside lysosomes
Autophagy
•Triggers PCD distinct from apoptosis if
can’t cope
• No caspase or CAD, chromatin laddering
• Occurs inside lysosomes
•Highly regulated!
Autophagy
•Triggers PCD distinct from apoptosis if
can’t cope
• No caspase or CAD, chromatin laddering
• Occurs inside lysosomes
•Highly regulated!
•Mis-regulation associated with heart
disease, diabetes and many more
Pyroptosis
PCD associated with
antimicrobial
responses in
inflammation
Pyroptosis
PCD associated with antimicrobial responses in inflammation
Toll-like receptors bind PAMPs, eg bacterial flagellins
Pyroptosis
PCD associated with antimicrobial responses in inflammation
Toll-like receptors bind PAMPs, eg bacterial flagellins
Activated NOD-like receptors (NLRs) initiate assembly of
pyroptosome
Pyroptosis
PCD associated with antimicrobial responses in inflammation
Toll-like receptors bind PAMPs, eg bacterial flagellins
Activated NOD-like receptors (NLRs) initiate assembly of
pyroptosome
Pyroptosome activates
Caspase-1
Pyroptosis
PCD associated with antimicrobial responses in inflammation
Toll-like receptors bind PAMPs, eg bacterial flagellins
Activated NOD-like receptors (NLRs) initiate assembly of
pyroptosome
Pyroptosome activates
Caspase-1
Caspase-1 executes cell,
Releasing PAMPs and
cytokines
Pyroptosis
PCD associated with antimicrobial responses in inflammation
Toll-like receptors bind PAMPs, eg bacterial flagellins
Activated NOD-like receptors (NLRs) initiate assembly of
pyroptosome
Pyroptosome activates
Caspase-1
Caspase-1 executes cell,
Releasing PAMPs and
Cytokines
Reason for depletion of
CD4 cells in AIDS
Necroptosis
PCD associated with viral infections
Necroptosis
PCD associated with viral infections
Infected cells release TNF
Necroptosis
PCD associated with viral infections
Infected cells release TNF
TNFR activates RIPK1
RIPK1 binds RIPK3 to form necrosome
Necroptosis
PCD associated with viral infections
Infected cells release TNF
TNFR activates RIPK1
RIPK1 binds RIPK3 to form necrosome
Necrosome activates MLKL
which permeabilizes membranes
Necroptosis vs apoptosis
Tend to inhibit each other, but do have overlap
Necroptosis vs apoptosis
Tend to inhibit each other, but do have overlap
Fail-safe for viruses that block apoptosis
Ferroptosis
PCD dependent on intra-cellular iron
Triggered by inhibition of cystine uptake
Ferroptosis
PCD dependent on intra-cellular iron
Triggered by inhibition of cystine uptake
Reduced cystine uptake leads to the production of lethal lipid ROS
Ferroptosis
PCD dependent on intra-cellular iron
Triggered by inhibition of cystine uptake
Reduced cystine uptake leads to the production of lethal lipid ROS
Erastin etc trigger it
Ferroptosis
PCD dependent on intra-cellular iron
Triggered by inhibition of cystine uptake
Reduced cystine uptake leads to the production of lethal lipid ROS
Erastin etc trigger it
Ferrostatin blocks it
Autophagy
– Plant PCD
• Changes in shape and position of
mitochondria (Mitochondrial morphology
transition, MMT)
• Nuclear condensation
• Condensation of PM from cell wall
• Deregulated: dev’l defects, lethality
MMT
(Scott & Logan, 2008, Plant Signaling & Behavior)
Plant PCD
In vegetative development
– Suspensor degradation during embryo devt
– Root cap devt and aerenchyma formation
– Shaping of leaves
Kawashima & Goldberg, 2009
PCD : Patterning in the lace plant leaf
http://www.youtube.com/watch?v=9gis4HK1XPg
http://completeaquarium.blogspot.com/2008/04/aponogeton-madagascariensis-lace-plant.html
PCD: aerenchyma formation
• Aerenchyma
–
–
–
–
Tissue for gas exchange
Aquatic species
Induced by submergence
Constitutive in rice:
adaptation to flooding
visible in all rice root
types, except in small
lateral roots
Rebouillat et al., Rice 2009
Plant PCD
• In vegetative development
– Tracheary element formation
PCD-specific hydrolytic enzymes accumulate
in vacuole
S1-nuclease
cysteine proteases
Vacuole enlarges
bursts
releases enzymes
autolysis of cell
contents & part
of cw
Plant PCD
• In reproductive development
–
–
–
–
Tapetum and stomium degradation in anther
Female gametophyte devt
Flower senescence
Incompatibility reactions
Model for integration of cytoskeletal events triggered by SI
Poulter, N. S., et al. Plant Physiol. 2008;146:1358-1367
Copyright ©2008 American Society of Plant Biologists
PCD : Evolutionary perspective
Developed independently?
Or evolved from a common
ancestral cell death process?
Some mol. components
-- conserved
e.g., PARP1,
Bax-inhibitor-1,
Defender against
Apoptotic
Death-1
http://bifi.unizar.es/research/pro_pro_inter_elec_transfer/research.php
PCD : Evolutionary perspective
• Caspases
– Cysteine proteases
– Mol switches that
activate c death
• Plants have proteases
w/ caspase-like
activities :
• Vacuolar processing
enzymes (VPEs)
Gao et al., Plant Signaling & Behav. 2008
PCD : role of mitochondrion
Mitochondria -sensor of death signals &
initiator of biochem
processes leading to cell
death
http://bifi.unizar.es/research/pro_pro_inter_elec_transfer/research.php
PCD : a role for chloroplasts
PCD occurs independently of chloroplasts
• Chloroplasts
– determine severity
of & number of cells
undergoing AL-PCD
– ROS
• Elevated levels –
physiological damage
• Signaling mol.
Gao et al., Plant Signaling & Behav. 2008
Cell death due to biotic/abiotic stress
Abiotic stresses:
Temperature extremes
Ozone
Hypoxia
Mediated by plant hormones
Ethylene
Jasmonic acid
Salicylic acid
Regulators:
Reactive oxygen species (ROS):
Superoxide anion radical
Hydrogen peroxide (H2O2)
Nitric oxide (NO)
Steffens and Sauter, Plant Cell, 2009