This document summarizes physiological and molecular mechanisms of aging and senescence in plants. It discusses that senescence is a natural process where organ function declines with age. This involves degradation of cellular components like DNA, proteins, lipids and organelles. Specific genes called senescence-associated genes (SAGs) are involved in breakdown of macromolecules while other genes are downregulated. Senescence can occur at whole plant, organ or cellular levels through programmed cell death. The document also discusses various triggers of senescence and usage of stay-green varieties with delayed senescence.

1. Physiological and Molecular mechanism of
Ageing and Senescence

2. Senescence
• Senescence or biological ageing is the change in the
biology of an organism as it ages after its maturity
• Such changes range from those affecting its cells and
their function to that of the whole organism
• The word senescence is derived from the Latin word
senex, meaning old man, old age, or advanced in
age
• Senescence: A program in which the function of
organ or whole plant naturally declines to death. This
is an essential phase of the growth and development
in plant

3. Ageing
Ageing is the accumulation of changes in an organism
or object over time
In biology, senescence is the state or process of ageing
Plant senescence is the study of aging in plants

4. Cellular senescence
• Cellular senescence is the phenomenon by which
normal diploid cells lose the ability to divide, normally
after about 50 cell divisions in vitro.
• Some cells become senescent after fewer
replications cycles as a result of DNA double strand
breaks, toxins, etc.
• This phenomenon is also known as "replicative
senescence", the "Hayflick phenomenon", or the
Hayflick limit in honour of Dr. Leonard Hayflick who
was the first to publish this information in 1965.

5. • In response to DNA damage (including shortened
telomeres), cells either age or self-destruct
(apoptosis-programmed cell death) if the damage
cannot be easily repaired.
• In this 'cellular suicide', the death of one cell, or more,
may benefit the organism as a whole.
• For example, in plants the death of the water-
conducting xylem cells (tracheids and vessel
elements) allows the cells to function more efficiently
and so deliver water to the upper parts of a plant.
• The ones that do not self-destruct remain until
destroyed by outside forces

6. Plants exhibit various types of
senescence
Senescence occurs in a variety of organs and in
response to many different cues.
Many annual plants, e.g. wheat, maize, soybean,
abruptly yellow and die following grain production.
Senescence of the entire plant after a single
reproductive cycle => monocarpic senescence

7. Monocarpic senescence in soybean
Left:
Entire plant underwent senescence
after flowering and production of
fruits.
Right:
Plant remained green and vegetative
because its flowers were continually
removed.

8. Other types of senescence
1. Senescence of aerial shoots in herbaceous perennials
2. Seasonal leaf senescence (e.g. deciduous trees)
3. Sequential leaf senescence (e.g. leaves die when they reach a
certain age)
4. Senescence (ripening) of fleshy fruit; senescence of dry fruit
5. Senescence of specialized cell types (e.g. trichomes, tracheids)
6. Senescence of storage cotyledons and floral organs

9. Stages of flower senescence in morning glory

10. Types of plant senescence
Overall Senescence
Senescence occurs in
whole plant body, such
as annuals which
senesces to death after
flower and setting.

11. Top Senescence
The part aboveground dies with the end of
growth season,but the part underground is
alive for several years.
Perennial weeds , corm and bulb lily
In summer In winter

12. Deciduous senescence
The leaf falls in summer or
Winter- Deciduous trees

13. Progressive senescence
Senescence only occurs in older organ or
tissue.New organ or tissue develops while
old those are senescing.

14. Simple model for leaf growth and senescence

15. •The involvement of different sets of genes during leaf senescence
affected by various senescence factors.
•Leaf senescence is affected by several factors and involves the
induction of different sets of genes.
•Apparent symptoms of senescence may look the same, the detailed
molecular states of senescent leaves are different depending on the
senescence factors.

16. Triggers of senescence
Internal → monocarpic senescence
External → day length and temperature in autumnal leaf
senescence of deciduous plants
→ abiotic and biotic stress
Regardless of the initial stimulus, different senescence
patterns share common internal programs in which,
regulatory senescence genes initiate a cascade of secondary
gene expression that brings about senescence and death.

17. Three stages of Leaf Senescence

18. Physiological and biochemical events
Senescence is genetically encoded, allowing a predictable course of
cellular events.
Some organelles are destroyed while others remain active.
Chloroplast – first organelle to deteriorate during onset of leaf
senescence (destruction of thylakoid protein components and
stromatal enzymes)
Nuclei remain structurally and functionally intact until the late
stages of senescence
Senescent tissues carry out catabolic processes that require de novo
synthesis of
• proteases
• nucleases
• lipases
• chlorophyll-degrading enzymes

19. Senescence is an ordered series of Physiological
and biochemical events
Senescence down-regulated genes (SDGs) – their expression decreases
during senescence
e.g. photosynthetic genes
Senescence-associated genes (SAGs) – their expression is induced during
senescence
Group A: proteases, ribonucleases, lipases, ACC synthase, ACC oxidase
Group B: glutamine syntethase (converts NH4
+
to glutamine, nitrogen
recycling from leaves)

20. Differential gene expression during leaf senescence
Senescence down-regulated genes (SDCs) include chlorophyll a/b-binding protein
gene (CAB), Rubisco small subunit gene (SSU).
SAGs - expression up-regulated during leaf senescence.
Class I SAGs - expressed only during senescence (senescence-specific).
Class II SAGs - have basal level of expression during early leaf development, but
expression increases during senescence.
Gan & Amasino (1997)

21. Physiological mechanism of Senescence on
Bio macromolecules

22. Physiology and biochemistry
Senescence-associated genes(SAGs)
Senescence is controlled by special genes.
Two kinds of genes can be found during senescence.
Senescence-downward genes most of genes code
enzymes relevant to photosynthesis, energy metabolism
and other synthesis.
Senescence-upward genes most of genes code enzymes
for hydrolase, such as DNase, RNase, Protease,
phospholipase

23. Senescence-associated genes SAGs refers to their
mRNA levels increase with senescence
proceeding. They function in metabolism of
biomacromolecule degradation and mobilization.
More than 40 genes have been cloned:
Proteases in Maize, A.thaliana,rape.
SAG2,LSC7,SAG12,LSC790,LSC760,RNS1,RNS2,RNS3
in A.thaliana ,
PEPC,MDH,MS,ICL,GAPDH,F-1,6-P, aldolase and
β—galactosidase in rape, corn and cucumber.

24. Degradation of biomacromolecules
1. DNA degrades RNA changes in quality and
quantity.
RNA break down faster than DNA does during
senescence, especially rRNA, which is more
sensitive to senescence.
RNase activity rises and DNA—RNA
polymerase activity declines.

25. 2.Protein synthesis decreases and its
degradation increases
Soluble protein-----Rubisco decreases by 85%,
thylakoid membrane protein decreases by 50%,
and cytochrome f,b also decreases fast
3. Biomembrane breakdowns and loses its
function.

26. Senescence is a recycling process
Some of the released nutrients (N)
such as nitrogen are transported to
developing seeds and young organs
at the shoot apex.
Senescence proceeds from leaf margins
toward the center. Cells surrounding the
vascular tissues senesce relatively late to
facilitate nutrient mobilization from
adjacent senescing cells.
Gan & Amasino (1997)
Plant Physiol. 113: 313

27. (a) Senescing leaves can be recognized by their characteristic loss of chlorophyll.
Often, the last areas of a leaf that senesce are close to veins, presumably because
these are needed for nutrient export.
The top-left leaf is just starting to senesce; the bottom-right leaf is in the most-
advanced stage of senescence.
(b) As a leaf senesce, nutrients such as nitrogen, phosphorus and metals are
reallocated to other parts of the plant such as developing seeds and leaves.

28. A model for regulatory pathways in
flower senescence
PCD signal is generated by both
external and internal stimuli and
transduced by some signals
resulting hormonal imbalance in the
cell
Altered level of hormones activates
several cascade and transcriptional
regulation
Initiation of senescence starts with
expression of several SAGs like
proteases, nucleases, wall
degrading and oxidative enzymes
Later stage of senescence
symptoms become visible and
ultimately leads to cell death of
flowers

29. Program for plant senescence
Senescence can occur at different levels:
-cell, tissue, organs and whole plant.
Cell senescence
Membrane and organelle senescence
Senescence in cell membrane
Lipid phase change
Biomembrane changes - liquid-crystalline state to
solid-gel state.
Hard and inflexible, fluidity decreases and cohesion
increases.

30. Degradation and peroxidation of lipid lead to
decrease in lipid content
Synthesis ↓, lipase ↑,
Phospholipase lipoxygenase and active O2 ↑
MDA (malonyldialdehyde) ↑

31. Phospholipid
↓ phospholipase A or B
Poly double-bound fat acid
↓ Lox (lipoxygenase )
Organic free radicals ---?

32. Biomembrane degradation and leakage.
Loss equilibrium of ions and disorder of
metabolism
Organelle senescence
Ribosome and rough ER↓
chloroplasts breakdown
mitochondria cristae swollen ↑
vacuole broken .
Autophagy occurs and cell senesces and
degrades.

33. Organ Senescence
Leaf senescence
Photosynthesis declines-----slower phase and
faster phase
Decrease in activity and content of photosynthetic
key enzyme (Rubisco)
Decrease in activity of photoelectron transport and
photophosphorylation.
Decrease in stomatal conductance.
Decrease in chlorophyll. Leaf yellow.
Organelle degradation

34. Impact of senescence on plastid ultrastructure in leaves of wild-type
and a stay-green mutant of the C3 grass X. Festulolium.
(A) Prior to senescence, the chloroplasts of a wild-type and mutant plants contain numerous
grana, stacks of appressed thylakoid membranes. (B) These internal membrane structures are
lost during senescence of a wild-type mesophyll cell, and electron-dense lipid droplets
known as plastoglobuli accumulate. (C) Retention of intrinsic thylakoid membrane proteins,
pigments, and other hydrophobic components gives the gerontoplasts of mutant tissues a
distinctive appearance, with persistent grana stacks and few plastoglobuli.

35. Chlorophyll a and its
breakdown products.
Subcellular compart-
mentation of the pheo-
phorbide, a pathway of
chlorophyll catabolism
in leaf mesophyll cells.

36. (A) Activity of key chlorophyll-catabolizing enzyme PaO (pheophorbide a oxygenase )is
strongly induced in senescing tissues of wild-type X. Festulolium but undetectable in
presenescent leaves and in a stay-green mutant.(B) Induction of chlorophyll degradation in
wild-type tissue is accompanied by loss of the pigment-binding membrane protein LHCP, as
shown by Western blotting analysis. In the mutant a second form of LHCPII progressively
accumulates as senescence proceeds. As illustrated in the cartoon, degradation of LHCPII
which protrudes from the thylakoid membrane into the stroma. (C) Stability of Rubisco, the
major stromal protein, is enhanced very slightly in the mutant compared to wild type.

38. Seed aging
The viability of seed loses inversely from mature to
death
Degradation and leakage of biomembrane:
Mitochondria and ER become swollen, plasmic
membrane contacts and depart from cell wall.
DNA injury broken
Enzyme activity decreases: dehydrogenase
Storage matter exhausting, free fat acid rising.

39. Programmed cell death is a specialized type
of senescence
Senescence can occur at the level of:
whole plant (monocarpic senescence)
• organ (leaf senescence)
• cell (tracheary element differentiation)
Process whereby individual cells activate an intrinsic senescence program
= Programmed Cell Death (PCD)
In animals, PCD may be initiated by specific signals (errors in DNA
replication during division)
- involves expression of a characteristic set of genes, resulting in cell
death
- accompanied by morophological and biochemical changes
(apoptosis, Greek: “falling off”)
- during apoptosis, cell nucleus condenses and DNA fragments in a
specific pattern

40. Programmed cell death is a specialized type
of senescence
PCD in plants, less well characterized
- PCD occurs during differentiation of xylem tracheary elements, during
which nuclei and chromatin degrade and cytoplasm disappears →
activation of genes encoding nucleases and proteases
- protection against pathogenic organisms
- infection by pathogen causes plant cells to quickly accumulate high
concentrations of toxic phenolic compounds and die (it’s not quite as
simple) → dead cells form small circular island of cell death (necrotic
lesion)
- necrotic lesions isolate and prevent infection from spreading to
surrounding healthy tissues by surrounding the pathogen with a toxic and
nutritionally depleted environment (hypersensitive response)

41. Programmed cell death (PCD)
The organism controls the initiation and execution of
the cell death process, these types of cell death are
referred to as programmed cell death (PCD)
PCD can appear in all organelles of cell

42. Cell death occurs in
almost all plant cells and
tissues.
PCD is involved in
numerous processes, including
the following illustrated in this
figure gamete formation,
including
Megaspore formation (1);
Embryo development(2);
Degeneration of tissues in the
seed and fruit (3);
Tissue and organ development
(4 ) through (6);
Senescence(7); and
Responses to environ-mental
signals and path-ogens(8 and 9).

43. The inflorescences of maize contain flowers that are initially bisexual, but PCD
results in the death of male or female tissues to give rise to female inflore-scence
(ear) or male inflorescence (tassel), respectively. In the tasselseed2 mutant
(A),female tissues in the tassel do not undergo PCD, and the resulting tassel flowers
are mostly pistilate. A wild-type tassel in included for comparison (B).

44. One visible example of PCD
in plants is seen in the
ornamental plant Mon-stera
deliciosa.
The leaves of this plant exhibit
deep indentations and hole in the
lamina, which result from the pro-
grammed death of specific regions
of tissue in the developing promor-
dia. As the leaf expands, these
areas are not replaced, and the
resulting leaf lamina has the
characteristic pattern that inspires
the common name, ‘‘Swiss cheese
plant’’

45. Utilization of germplasm resistant to
senescence
selection of varieties and cultivars resist to
senescence
Transgenic plant for resistant to senescence
ACC synthase gene, nr, (ipt1, kn1)
Control of senescence

46. Tobacco plants over-expression of the kn1 gene
• Overexpression of kn1 in
Tobacco
• 35S:kn1 plants are
characterized by a reduction
in leaf and plant size,altered
leaf shape,loss of apical
dominance, delay in
senescence, and formation of
ectopic meristems. At left is
a leaf from a nontransformed
plant; at right is a 35S:kn1
branch.

47. Salicylic acid has a role in regulating gene
expression during leaf senescence
Morris et al. 2000
Plant J 23: 677
pad4
Arabidopsis mutants defective in SA-signaling:
npr1 = NONEXPRESSER OF PR GENES 1 (ankyrin repeat protein)
pad4 = PHYTOALEXIN-DEFICIENT 4 (lipase-like protein)
NahG = expresses salicylate hydroxylase, unable to accumulate SA
As leaves started to senesce, chlorosis became
visible at the edges, gradually spreading up the
leaf. This chlorosis was rapidly followed by
necrosis, the senescing tissue normally dying well
before the entire leaf became chlorotic.
Plants grown at 12h L/8h D.
pad4 showed uniform chlorosis over the
entire leaf lamina, but negligible signs of
necrosis.
Effect of pad4 mutation appears to be to
delay or even inhibit necrosis in the
senescing tissue.