In this article we will discuss about Senescence. After reading this article you will learn about: 1. Patterns of Senescence 2. Physiological Changes During Senescence 3. Control.
Patterns of Senescence:
Senescence in plants shows a wide range of Patterns.
(i) Cellular Senescence:
Individual cells or a small number of cells of an organism may undergo senescence while the other cells do not. Both gametogenesis and embryo development involve orderly sequences of cellular senescence. During female gametophyte formation, three out of the four cells produced by meiosis degenerate. The synergids and the suspensor cells also senesce during embryo growth.
(ii) Tissue Senescence:
In many circumstances, large groups of cells or tissue may disintegrate and die. The tapetum, i.e., the layer of cells that surrounds the microsporocyte cells or pollens degenerate, while the nucellar layer next to the growing embryo may also break down.
The senescence of groups of cells in particular locations may play a role in leaf morphogenesis. Through lysigenous process, root cortex cells, pith cells and even mesophyll cells may form aerenchyma cells with air spaces.
In addition, mechanical events like tearing and detachment of branches from the plant cause tissue death through deprivation of nutrient supply. During abscission of plant parts, specialized layers of cells, abscission zones, are differentiated preparatory to separation and this is the senescence process. Formation of xylem tracheids or vessels which are devoid of protoplasm is also a case of senescence.
(iii) Organ Senescence:
Even a single organ may follow diverse patterns of senescence which is exemplified by leaves. Leaf senescence may be progressive, the older leaves senesce as new leaves are produced. In monocarpic senescence, however, all the leaves may senesce more or less at a time. Foliar senescence may also be synchronous on a seasonal basis. Even within a leaf, the cells may senesce at different times and rates.
Some leaves senesce from the apex towards the base, while senescence in others starts over the main veins showing vein yellowing and then continues in the interveinal regions. The senescence of leaves and branches in response to environmental stress represents an adaptation either to reduce the water evaporative surfaces or to allow better light perception by the plant.
(iv) Organism Senescence or Whole Plant Senescence:
Annual and biennial plants are monocarpic showing post-reproductive death, while the perennials are generally polycarpic. Monocarpic plants have one reproductive phase followed by death and polycarpic plants have more than one reproductive phase before death. It is convenient to call the death of monocarpic plants, especially, field crops, as monocarpic senescence.
Whole plant senescence is accompanied or preceded by a decrease or cessation of both shoot and root growth. The reduction in vegetative growth occurring during the reproductive phase has been recognized for a long time in both monocarpic and polycarpic plants. Where the shoot apex is converted to an inflorescence as in corn and Xanthium, node production ceases coincident with the appearance of flower buds.
In soybean, cotton and pea, stem elongation decreases after flowering has started and stops when the fruits are growing. Root growth may be affected early in the reproductive development which may be due to a nutrient deficiency resulting from a large-scale diversion of nutrient supply to developing fruit.
Thus in whole plant senescence, the control centres for growth cessation are the reproductive structures. In most cases, removal of reproductive sinks like defloration or de-fruiting or de-budding has been found to restore vegetative growth.
Physiological Changes During Senescence:
All the physiological processes decline during senescence and a multitude of changes lead to death. In this respect, most of the biochemical work deals with changes occurring in the leaves either as detached organs or attached in whole plants.
(i) Photosynthesis:
It is generally observed that the net photosynthetic rate increases as leaves grow and then declines gradually at the time of maximum leaf expansion. This indicates that the rate of photosynthesis is a function of individual leaf age.
During the rapid phase of whole plant senescence, young and old leaves degenerate almost together. The rate of photosynthesis also declines with equal rapidity in young and old leaves. Simultaneous senescence of leaves occurs not only in monocarpic senescence but also in autumnal senescence of polycarpic plants.
Although loss of chlorophyll content is a commonly used index of senescence, it does not always measure accurately either senescence or photosynthetic activity.
Chlorophyll content usually decreases well after photosynthetic activity has begun to decline, and in some cases, chlorophyll content shows an increasing trend while the photosynthetic activity is dropping. Even then, chlorophyll loss during senescence offers a visual method of estimating the degree of senescence.
As with chlorophyll content, the synthesis and activities of chloroplast enzymes (e.g., RuBPcase) decline after the cessation of leaf growth which is parallel to the loss of photosynthetic activity. Batt and Woolhouse , demonstrated that the Calvin cycle enzymes that are synthesized on chloroplast ribosomes decline earlier during senescence than those synthesized primarily on cytoplasmic ribosomes.
It has been shown that conformational changes and loss of active site leading to the loss of RuBPcase occur at a faster rate than the breakdown of total Fraction I.
Although photorespiration does not show a uniform pattern of change in all aging plants, it increases greatly in senescing C4 plants, and the increased photorespiration, a characteristic of C3 plants, may be related to a shift to C3 type CO2 fixation. Thus, it appears that the overall decrease in photosynthetic rate in senescing leaves results from a decline in CO2 reduction reactions.
(ii) Respiration:
The respiratory apparatus of senescing tissue remains active until late in senescence, and then declines rapidly. Loss of respiratory capacity can be a factor in the final stage of senescence, whereas there is evidence that the initial stage of senescence is not linked with respiratory decline.
The mitochondria often swell and decrease in number, but these changes occur late in senescence. Amino acids have been found to accumulate, giving rise to a change in the respiratory quotient. A climacteric rise in respiration may occur in the senescence of both intact and detached leaves.
From the fact that respiration decreases only late in senescence and that the lack of oxygen supply prevents the breakdown of chlorophyll and protein, it appears that cellular energy is required during senescence, possibly for the synthesis of the degradative enzymes. The respiratory climacteric of senescing leaves is correlated with a rise in RNA levels and an increase in protease activity.
(iii) Nitrogen Fixation and Mineral Uptake:
Several studies have demonstrated that symbiotic nitrogen fixation in legumes directly depends upon the amount of photosynthetic available to the root nodules. It is interesting to note that depodding which increases the availability of photosynthetic can cause appreciable increase in nitrogen fixation and delay nodule senescence.
In a similar way, the decline in whole plant photosynthesis parallels the decline in nitrogen fixation. Symbiotic nitrogen fixation decreases with the aging and senescence of leguminous plants. Such decline in nitrogen fixation is associated with the structural changes of individual nodules and bacteroids which is followed by their senescence.
Root growth as well as root function usually slow early in the reproductive phase, lust like nitrogen fixation, mineral uptake through the roots suffers a decline during the reproductive phase.
(iv) Protein and Nucleic Acids:
The most basic of all events accompanying senescence is the decline in protein and nucleic acid levels. It has been shown that although there is a decline in protein, RNA and DNA of senescing tissues, these three metabolites do not decline at the same rate.
There is an early gradual decline in protein and RNA about the time when vegetative growth ceases, while DNA decreases last. The initial decrease in protein and nucleic acid in the chloroplast involves a decrease in the major chloroplast enzyme. RuBP case and other enzymes which are synthesized on chloroplast ribosome.
The loss of these enzymes is correlated with reduced ability of the chloroplast to synthesize protein and RNA coupled with a reduction in the number of chloroplast polysomes.
The decline in protein and nucleic acids takes place in two stages. The period of gradual decline, characteristic of initial stage of senescence, is followed by more rapid senescence and rapid decline when chlorosis or leaf yellowing starts. During the rapid decline, protein and nucleic acid degradation is accelerated in both the chloroplasts and the cytoplasm.
In addition, the synthetic capacity in the whole cell decreases. During this period, large quantities of hydrolytic enzymes like protease, RNase, phosphatase and chlorophyllase are synthesized on cytoplasmic ribosome.
Thus, the prime candidates for central centres for a marked decline in protein and nucleic acids seem to be due to (a) release or activation of hydrolases present in the vacuoles or lysosomes, (b) a possible decrease in protease inhibitor, and (c) a decrease in protein and nucleic acid synthesis.
In the whole plant, the senescing leaves before their abscission are depleted of materials like amino acids, sugars which are transported to other parts.
(v) Membranes and Organelles:
Of all the cell organelles, the chloroplast shows the earliest symptoms of physiological decline. Decrease in RuBP case activity is noticed first with a corresponding early loss of chloroplast ribosomes and this precedes the decrease in cytoplasmic ribosomes. In later phases of senescence, however, pronounced ultra-structural changes in the thylakoids occur.
Other changes occurring at this time include swelling, vesiculation and disappearance of endoplasmic reticulum (ER) and Golgi bodies together with the loss of ER-associated ribosome.
The galactolipids and sulpho-lipids, the constituents of chloroplast lipids, decrease before the phospholipids that predominate in the non-chloroplast membranes, suggesting that the biochemical decline may occur relatively early in chloroplasts. Although the changes in chloroplasts occur early, they remain intact till the time when the tonoplast ruptures.
As soon as the tonoplast disintegrates, the hydrolytic enzymes, acids and toxic compounds are released in the vacuole and this triggers the cellular degradation. In the final stage of cellular degradation, the plasma lemma disintegrates and the nucleus undergoes massive alteration, whereas the mitochondria may persist with intact shape even at this stage.
It is generally acknowledged that membranes seem to play an important role in plant senescence.
(vi) Nutrient Deficiency Syndrome:
Nutrient deficiencies may be important in the senescence programme of particular organs or the whole plant. This concept finds support in the senescence of monocarpic plants where the emergence of reproductive structures like flowers and fruits seems to impose a great demand on the vegetative body, thus causing nutrient deficiency.
In such cases, the life of the plant can be spared or at least death can be delayed by removal of the reproductive structures, obviously, through avoidance of nutrient deficiency.
At present, it has been possible to recognize two patterns of deficiency:
(i) Nutrient drain or withdrawal from the senescing parts
(ii) Diversion of the supply of nutrients away from the senescing organs
Thus, nutrient deficiency seems to be the primary cause of monocarpic senescence. Deficiency caused by nutrient drain, e.g., mineral withdrawal, and nutrient diversion, e.g., mineral and cytokinins from the roots and photosynthetic produced by the leaves, presumably play a role in monocarpic senescence.
Control of Plant Senescence:
(i) Hormones and Senescence:
Senescence of higher plants are genetically and environmentally regulated processes intimately associated with hormonal interactions. The external applications of plant hormones have been found either to promote or to retard senescence. The well-known senescence-promoting hormones are ethylene and abscisic acid, whereas senescence-retarding hormones include cytokinins, auxins and gibberellins.
(a) Ethylene:
It is the most active senescence-promoting plant hormone is unique in that it is a simple gaseous hydrocarbon. Ethylene is produced by most higher plants in trace amounts and influence many aspects of plant growth, including aging and senescence.
Studies that prove ethylene to be a promoter of senescence can be divided into two main groups, those showing the effects of exogenous ethylene and those indicating the role of endogenous ethylene.
Numerous studies have demonstrated that ethylene is a fruit-ripening hormone. The onset of ripening and senescence coincide with an increase in ethylene production which triggers many metabolic processes, characteristic of ripening.
Fruit-ripening and senescence phenomena that are mediated by ethylene are associated with:
(i) Changes in the rate of respiration
(ii) Changes in membrane permeability
(iii) Destruction of chlorophyll and synthesis of chromoplasts and carotenoids along with non-plastidial pigments like anthocyanin
(iv) Metabolic shifts involving carbohydrates, proteins and organic acids
(v) Textural changes and softening of tissue
(vi) Development of flavour and aroma.
Besides the studies on the phenomenon of fruit ripening as a specialized model of organ senescence, much of our knowledge of plant senescence is derived from studies on leaves. As a developmental process, the senescence phenomenon seems to be genetically programmed for optimum advantage for the plants.
For instance, increased protein breakdown during senescence provides amino acid that are exported from the senescing leaves to other plant parts either for their reutilization or for storage as reserve nutrients.
Besides this, abscission of leaves reduces the rate of transpiration in drought conditions. Exogenous ethylene can accelerate many of the physiological changes normally associated with leaf senescence. Ethylene treatment has been shown to result in increased activities of many hydrolytic enzymes like cc-amylase acid phosphatase, ATPase, chitinase, β – 1, 3-glucanase, pectin-esterase and cellulase.
A remarkable stimulatory effect of ethylene on respiration in senescing leaves has been noticed. Excised leaves of Hedera helix can be maintained in darkness for months without undergoing senescence, but they senesce rapidly following exposure to ethylene.
Flower tissues respond to ethylene treatment by reduction of RNA content, increased RNase activity and changes in membrane permeability.
Several observations that implicate ethylene as a natural enhancer of senescence indicate that sudden increase of both ethylene production and respiratory CO2 is found to coincide with rapid chlorophyll destruction. There seems little doubt that a natural rise in ethylene production and evolution regulates a number of events during early stages of leaf senescence.
The process of abscission occurs as a result of cell-wall breakdown in the separation layer formed within the abscission zone. Ethylene is a potent accelerator of abscission. The target cells in the abscission zone undergo enlargement prior to abscission and this expansion of cells is induced by ethylene.
The activities of cell wall degrading enzymes like cellulase and polygalacturonase, found in the abscission zone region, increase in response to ethylene .
(b) Abscisic Acid:
Next to ethylene, ABA is the most promising of the senescence promoters. ABA promotes chlorophyll loss in detached leaves and leaf discs. On the other hand, the effect of ABA on attached leaves is generally less pronounced. ABA sprays have no effect on leaf senescence, suggesting that ABA has little effect on attached leaves.
The possible reasons for this difference between attached and detached leaves, are poor uptake, rapid translocation, inactivation and interaction with other endogenous hormones. It has been established that ethylene functions as a promoter of flower senescence. In some cases, however, ABA, particularly at high concentration, e.g., 10-4M has been found to retard senescence in leaf discs.
In senescing tissue, ABA has been reported to accelerate RNA and protein loss and ABA elevates protease and nuclease activity either through increased synthesis or by enzyme activation. The endogenous concentrations of ethylene have been found to rise during fruit development and maturation.
There are evidences that increased ABA levels may play an important role in inducing senescence of the whole plant (e.g., monocarpic senescence), but the exact relationship is yet unknown.
(c) Cytokinins:
It plays an important role in controlling many processes that contribute to plant senescence. The early observation by Richmond and Lang that cytokinins inhibit senescence through the maintenance of protein and nucleic acid levels has led to the general idea that cytokinins delay senescence by maintaining or promoting protein and nucleic acid synthesis.
Since the roots are the major source of leaf cytokinins, roots are important in regulating leaf senescence. Generally, cytokinins are most effective when applied to detached plant organs, but they can also delay senescence of attached leaves. Thus, treatments and environmental factors which alter root activity and cytokinin production may exert effects on cytokinin levels and leaf senescence.
The senescence of green leaves involves changes in their photosynthetic apparatus and chlorophyll breakdown is a conspicuous parameter for the measurement of leaf senescence. Since cytokinins are very effective in delaying chlorophyll breakdown, it is apparent that cytokinins are involved in maintaining the photosynthetic apparatus of plant organs.
Cytokinin treatments increase chloroplast DNA, promote chloroplast protein synthesis, maintain pigment levels, alter membrane permeability, promote chloroplast replication and grana formation.
Cytokinins may selectively increase the levels of certain photosynthetic enzymes, it is not clear whether the enhanced activity is due to greater synthesis, inhibition of degradation or activation of preexisting enzymes.
It has been suggested that cytokinins exert their effect on chloroplast metabolism indirectly through action on the nucleus or cytoplasm. Cytokinins increase chlorophyll levels, but it is not clear whether cytokinins act by stimulating chlorophyll synthesis or by inhibiting its breakdown.
However, cytokinins have been reported to reduce the activity of chlorophyllase, which degrades chlorphyll and thereby chlorophyll level may be raised. Cytokinin also prevents the rise in certain RNases and proteolytic enzymes which are normally related with senescence.
The movement of assimilates has been found to be regulated by cytokinins. Mothes and Engelbrecht and Mothes etal., were the first to indicate that the cytokinins can influence nutrient redistribution in detached leaves. In excised leaves, nutrients are not only retained at the site of cytokinin application but they move from untreated parts to treated areas of the leaf.
This will lead to delay in senescence of the treated parts and acceleration of senescence in the untreated parts.
(d) Auxin:
Both synthetic and natural auxins can delay senescence in a wide range of tissues. Auxins delay senescence by altering processes related to senescence such as chlorophyll loss, RNA degradation, RNA synthesis, protein degradation, protein synthesis, wilting and membrane breakdown.
Auxins, however, may promote senescence in some cases, such as xylem differentiation and flower petals. It has been shown that xylem regeneration in stems is induced by auxin coming from nearby leaves. Auxin promotion of ethylene production in a number of flowers may result in petal senescence.
(e) Gibberellins:
Most of the studies concerning GA effect on senescence show that chlorophyll loss in leaves can be retarded by GA applied exogenously.
Exogenous GA can inhibit many other senescence-related processes, such as RNA and protein breakdown. In some cases, GA effects on such processes are quite diverse indicating that they may not be closely linked.
For example, loss of chlorophyll is retarded by GA in some cases like Rumex, Nasturtium while others like bean, peanut, Taxodium show promotion of chlorophyll loss and there are still others like tobacco, barley, radish where GA appears to exert no effect.
Endogenous GA activity has been found to decline during senescence in a wide variety of tissue. For all types of tissue showing a decline in endogenous GA activity, exogenous GA delays senescence which suggests that a decline in GA plays a role in senescence.
(ii) Senescence in Monocarpic Plant:
Since monocarpic plants degenerate following their reproductive phase, anything that delays flowering should postpone monocarpic senescence. One of the major components of monocarpic senescence is the cessation of vegetative growth. The decline in vegetative growth, viz., the production of new leaves naturally prevents the renewal of these assimilatory organs and obviously results in decline in photosynthesis.
This reduction in organ formation is also closely linked with decreased cambial activity and the result is a less active phloem tissue. Prevention of flowering and de-fruiting may allow monocarpic plants to attain a much greater size and age than normal which signifies an antagonism between vegetative and reproductive growth.
Even though reduction in leaf production and root growth occurs with decline in assimilatory processes early during the reproductive phase, some difference in assimilation in the roots and leaves is apparent. During monocarpic senescence, the leaves show decrease in a wide range of physiological functions of which the decline in photosynthesis is the most important factor.
On the other hand, root assimilation may decline ahead of photosynthesis. This obviously would lead to changes in translocation of the photosynthetic, i.e., preferentially to the reproductive structures at the expense of the roots.
If we look at the drastic decrease or total cessation of vegetative growth coincident with the increase in reproductive growth, two aspects seem to play a causal role in monocarpic senescence:
(i) A shift (nutrient diversion) in the partitioning of the photosynthetic away from the roots to the developing fruits
(ii) Competition between leaves and fruits for mineral nutrients assimilated by the roots.
A simple but attractive explanation is that developing fruits play a prominent role in monocarpic senescence since they act as sinks that drain the rest of the plant by their greater consumption. From the observation that a massive loss of metabolites from the leaves occurs with their concomitant appearance in the fruit of monocarpic plants, it is tempting to consider monocarpic senescence as exhaustion death.
Death of the individual cells of an organ as a component of an organism may be due to the fact that they are selectively targeted to die, or because they are parts of an organ or organism that is undergoing senescence. Thus the causal mechanism of whole-plant (monocarpic) senescence is to be analysed in terms of the control centres and target organs.
We have to understand which structures act as inducers of senescence and which are the responding organs. It has been known for a long time that reproductive development and monocarpic senescence are tightly coupled and thus removal of reproductive structures can prevent or delay monocarpic senescence.
To answer the question of which primary target is influenced by reproductive structures, experiments with soybean indicate that the reason for plant death is leaf senescence. The leaves appear to be the primary target of the influence exerted by the fruit. The role played by the root system and the stem are only secondary and supporting.
It appears that during pod maturation, leaves no longer supply nutrients and hormones to the roots which decline in activity and ultimately the whole plant dies. Lindoo and Nooden, called the influence of the reproductive structures on the vegetative parts the ‘senescence signal’.
The information available on the behaviour of the senescence signal in species like soybean indicates that the seeds seem to be the source at least in bisexual plants. The senescence signal is exerted mainly on the leaf closest to a pod and beyond this, it travels mainly downward.
The senescence signal is probably a hormone produced by the fruit (seeds) that promotes senescence in the remaining part.
One problem with the senescence hormone theory is the difficulty to conceive that something (e.g.. hormone) is flowing out of an active sink, such as a growing fruit, but recent work indicates that outward transport of materials occurs across the seed coat.
The well-known senescence promoters like ethylene and/or abscisic acid may be the senescence signal for monocarpic senescence. In addition, a variety of natural products like methyl jasmonate, serine, aliphatic alcohols and fatty acids such as linolenic acid are possible candidates for a senescence hormone.