PLANT PHYSIOLOGY SENESCENCE MECHANISM

BY: RINI SANTIKA 54892/2010 BIOLOGY EDUCATION

BIOLOGY DEPARTMENT MATHEMATICS AND NATURAL SCIENCE FACULTY PADANG STATE UNIVERSITY 2012

PREFACE Thanks to Allah SWT that give us bless, health, and opportunity to finished this manuscript in right way and right time. And thanks for our lecture Dr. Azwir Anhar, M.Si that has guided us in the course Plant Physiology and especially for all friends that give me motivation and support among this manuscript written. I hope this manuscript can help people to understand about senescence mechanism in plant. I know and understand that my manuscript still have mistake and need fix to be perfect. So that we accept critics and advise to fix this manuscript. Thanks for all.

Padang, November 2012

Rini Santika

CHAPTER I INTRODUCTION

A. Background

Processes of deterioration that accompany aging and that lead to death of an organ or organism are called senescence. Although meristems do not senesce and might be potentially immortal, all differentiated cells produced from meristems have restricted lives. Senescence therefore occurs in all

nonmeristematic cells, but in different times. In evergreens, many species retain their leaves for only two or three years before they die and abscise. In deciduous trees and shrubs, the leaves die each other , but again the stem and root system remain alive for several years. In perennial grasses and herbs such as alfalfa,the aboveground system dies each year, but the crown and roots remain largely viable. In herbaceous annuals, leaf senescence progresses from old to young leaves, followed by death of of stem and roots after flowering. Only the seed survives.

B. Problem formulation 1. How does pattern of aging and death ? 2. What does the metabolic aspects of senescence ? 3. How does nutritional competition in senescence ? 4. What is the effects of growth factors in senescence ? 5. What causes senescence ?

C. Purposes 1. Understand pattern of aging and death 2. Understand the metabolic aspect of senescence 3. Understand nutritional competition in senescence 4. Understand the effects of growth factors in senescence 5. Understand the causes of senescence

D. Limitation of Issues 1. Explain the pattern of aging and death 2. Explain the metabolic aspect of senescence 3. Identify nutritional competition in senescence 4. Explain the effects of growth factors in senescence 5. Identify the causes of senescence

CHAPTER II EXPLANATION

The breakdown of cell components and membranes that eventually leads to the death of the cells is called senescence. The leaves of deciduous trees and shrubs senesce and drop through a process of abscission every year. Even evergreen species often retain their leaves for only 2 or 3 years and the aboveground parts of many herbaceous perennials senesce and die at the close of each growing season.

Why do plant part senesce? Some studies have suggested that certain plants produce a senescence factor that behave like, or is actually, a hormone, but we are not yet certain of the precise mechanism involved. We do know, however thet both ABA and ethylene promote senescence. On the other hand auxin, gibberellins, and cytokinins delay senescence in a number of plants that have been studied. Other factors such as nitrogen deficiency and drought, also hasten senescence. (Carl L, 1962 : 196)

1. Pattern Of Aging And Death

Plants and their parts develop continuously from germination until death. The latter part of the development process, wich leads from maturity to the ultimate complete loss of organization and function, is termed senescence. It is a characteristics of plant behavior that senescence is not simply a running down of the life process but it is a highly ordered and programmed process. Plants do not go to pieces as they age. They age, as they grow and develop in an orderely fashion.

Plants, according to their habit of growth, senesce in many different ways. The whole plant may senesce and die at one time, as occurs in many annuals after flowering is complete. Alternatively, there may be a progressive senescence of parts as the whole plants age-some parts (usually those nearest the tips of shoots and roots) remaining active and in the juvenile stage while the older parts (particularly older leaves) senesce and die. Third there may be simultaneous senescencence of a part of the plant, while the rest of the plants remains alive. Finally during the process of tissue maturation certain cells, such as xylem vessels and tracheids or sclerenchyma tissue, may senesce and die although the plant as a whole is in a stste of vigorous growth.

Pattern of senescence appear to differ in quite important ways, both in their causes and in the nature of the senescence process, as well as in their degree of reversibility. Some types of senescence appear to be closely correlated with developmental events in the whole plants. For example, senescence in monocarpic plants (those that flower only once and then die) is closely related to the process of flowering and the growth of fruits. If flower or fruits are removed, senescence may be postponed for many years. Some monocarpic plants do indeedlive for many years before flowering, but when they have produce fruits, they die.

2. Metabolic Aspects of Sensescence

At the cellular level, senescence appears to be tightly controlled, although the mechanism of controls are not unknown. Senescing cells undergo reduction of their structure, and much of the membranous subcellular, inclusions are disrupted. It has been suggested that the vacuole acts as a lysosome, secreting hydrolytic enzymes, whish digest cellular material that is no longer needed. Evidently some sort of breakdown of the tonoplast takes place, and hydrolytic enzyme are liberated into the cytoplasm. However, the situation is not so simple because the internal structure of the chloroplast and mitochondria is also reduced, and this seems to happen before their external membranes are breached. Therefore, it seems likely that degradative processed are initiated, or synthetic processed eliminated, in organelles as well as in cell. Possibly the same signal that cause senescence in cells is also perceived by their organelles, causing them to senesce simultaneously.

3. Nutritional Competition In Senescence.

The german physiologist H. Molisch suggested in the 1920s that senescence might be caused by nutritional deficiencies. Different part of the plant compete for nutrition, and fruit or growing tips, for example, might form stronger sinks for translocation and thus accumulate so much of the available nutrient that older leaves would be starved. He pointed out that, if the fruit, seeds, or growing tip is removed from plants, senescence of other parts such as leaves is greatly delayed. This theory can be accommodated to later ideas about hormone direction of translocation if it is postulated that starvation of older leaves is due to the direction of translocation by hormones produced in the growing tips or developing fruits. The effects of cytokinins, which delay or prevent senescence when applied to a leaf, might be to cause cell divisions, possibly accompanied by IAA production, which would then act to direct translocation toward the area of its production.

4. Effects Of Growth Factors

A clue to the causes of senescence came from the observation that if a detached, senescing leaf begins to form roots, then senescence is reserved. This suggested that root produce something that is translocated to leavesnand prevents or reverses senescence. Scientist working in both America and Germany discovered that cytokinins applied to leaves would would reverse senescence in the area of the leaf to which they were applied. Later work showed that roots do indeed produce cytokinnins and it has now become reasonably certain that the antisenescence hormone translocted from roots in fact a cytokinin or a group of cytokinin or a group of cytokinins.

The mechanism of action of cytokinin is not wholly clear, but there are indications from Mothes experiments. He found that when a drop of kinetin or other cytokinin is placed on a leaf, various organic and in organic nutrients are mobilized in peripheral areas of the leaf and move into the kinetin-trated area. It is not clear whether the increased nutritions id the immediate cause of rejuvenation and

mobilization of nutrients.

The question may be asked: why do certain (that is, older ) leaves on an intact plant senesce, whereas younger leaves do not? Both apparently have the same access to the root system. The answer may be lie in ther fact that nutritional traffic in the plant tends to be strongly directed toward younger and more actively growing parts of the plant. This directions of translocation is possibly the result of more vigorous auxin production in rapidly growing tissue; auxin has been shown to increase translocation toward the site of their application or production.

The movement of cytokinin from the cytokinin from the root may be affected in the same way; thus, senescence may be the result of the starvation of older leaves, not only of nutrients but of cytokinin also. The addition of the cytokinin benzyladenin has been shown to prevent senescence in older leaves of bean plants. This suggest that the causes of senescence is indeed a lack of cytokinins.

As usual, there are complications. Not all plants respond to the same hormones. Cytokinin appear ti be more affective in many herbaceous plants. Gibberellins are effective in retarding senescence of the dandelion (Taraxacum officinale) and the ash (Fraxinus), and the endogenous gibbereliin levels fall progressively during leaf senescence. Auxins (IAA and 2,4-D) have been found to retard senescence in certain trees, although they cannot always be shown to have this effect in all plants. Ethylene strongly promotes senescence in many tissues; it

appears to be physiologically involved in ripening fruits, in which its concentration may be build up to effective physiological levels. There is strong evidence to suggest that ethylene is intimately connected with aging. It has a strong phytogerontological effect if applied externally. The American physiologist A. D. Hanson and H. kende have shownthat ethylene is derived largely or exclusively from the amino acid methionine. Methionine is also involved in methylation ractions, which keep its concentration low in young, actively growing plants. As activity decreases the methionine content builds up greatly and ethylene synthesis tajes place. The inference is that the ethylene may be an integral part of the aging process, but does not cause it. The ultimate cause of aging is still unknown. (Bidwell, 1979 : 546-551)

5. Causes of senescence

What causes senescence? Chemical analyses show that leaf senescence is accompanied by early losses in chlorophyll, RNA, and proteins, including many enzymes. Because these and other cellular constituent are constantly being synthezised and degraded, loss could result from slower synthesis or faster breakdown, or both. Slow synthesis is expected when nutrients normally arriving in an organ are diverted elsewhere, as, for example, whe flowering and fruit formation occur. One theory for leaf senescence is, therefore, that flower and fruit development cause a competition for nutrients.

Source : sciencedirect.com

Contrary to effects of the hormones, ethylene and ABA promote senescence. In fruits the effect of ethylene is manifested by rapid ripening followed by abscission; in flowers, the common result is fading, transport of nutrients, withering, and then abscission, while in leaves we observe loss of chlorophyll, RNA and protein, and transport of nutrients, followed by abscission. The effect of ethylene seems to us much more dramatic than that of ABA. To what extent natural rises in the ABA levels contribute to senescence and abscission is still uncertain.

What advantage is there to abscission of senescence leaves, flowers, and fruits? For fruits, the importance in perpetuation of the species is obvious, because fruits contain seeds. For flowers, we suspect that the reason involve removal of a useless organ that might act as potential infection source and that, in some species, would shade new leaves the next growth season. Senescence of flower is usually accompanied by hydrolysis of RNA and protein. The products are converted into mobile amides and amino acids. Many other large molecules (except for those in cell wall) are also degraded into smaller, more readily translocatable form in which nutrients are conserved by storage in othe parts of the plant. For leaves that abscise, a similar extensive salvage of nutrients by mobilization also precedes abscission.

This nutrient economy helps forest trees to survive on unfertile soils. Leaves that abscise apparently could not with stand cold winters and would shade new leaves the next spring, so their loss, preceded by nutrients salvage, increases survival and productivity of individual perennial plants.

In most species, abscission of leaves, flower, or fruits is preceeded by formation of an abscission layer or zone at the base of the organ involved. In leaves, this zone is formed across the petiole near its junction with the stem. In many compound leaves, each leaflet also forms abscission zone. The abscission zone consist of one or more layers of thin-walled parenchyma cells resulting from

anticlinal divisions across the petiole. In some species, these cells are formed even before the leaf is mature. Just before abscission, the middle lamella between certain cells in the distal region of the abscission layer is often digested. This digestion involved synthesis of polysaccharides-hydrolyzing enzymes, most importantly cellulose and pectinases, and their secretion from the cytoplasm into the wall. Formation of the enzymes is accompanied by a rapid rise in respiration in cell of the proximal part of the abscission zone (bthose cell of the zone close to the stem). This rise is similar to that which occurs in climacteric fruits and also involves increases in polyribosomes characteristics of cell actively synthesizing proteins. Furthermore, one or more layers of these proximal cells increases in size (both length and diameters), while the cells of the abscission zone distal to the breaking point do not. These wall digestion processes accompanied by pressure resulting from unequql growth in expanding proximal and senescent distal cells of the zone apparently cause a break between them. Ethylene causes cell expansion and secretion of the cell-wall degrading hydrolases in some species.

Several environmental factors promote abscission, especially drought and nitrogen deficiency, but these first hasten senescence. Eventhough abscission is an active process in cell proximal to the break, the organ being shed nearly always first comes senescent. What role do hormones play in abscission? Our present ideas about leaves are summarized as follows: An auxin is synthesized in growing leaf blades and strongly retards senescence and abscission until its level and rate of transport into the petiole decrease too much when the leaf matures. Cytokinin and perhaps also gibberellins arriving from the root also delay senescence and abscission for a while. Finally, however, degradation processes overcome synthetic processes in the leaf, partly because of competition with growing organs for nutrients, and senescence occurs. Now something, perhaps senescence factor, causes ethylene production in the abscission zone, and ethylene stimulates growth of the proximal cells and formation of cell wall degrading enzyme in them. Abscission then occurs. No clear cut role

ABA in this sequence has been established, although increases in ABA might contribute to the senescence preceding abscission and abscission itself.

You should now realize how far we have departed from Julius von Sachs early idea that plants might have specific hormones responsible for growth or formation of particular organ. Clearly, the rule is most physiological processes require interactions among several hormones, and a single hormone has several function. Furthermore each process generally depends on the kind of cells involved and on the species. Apparently, different species sometimes use different interactions among them to accomplish their various function.

Furthermore, other hormones await discovery. There is evidence for a hormone that moves from leaves to underground stems, where it causes tuber and bulb formation, for a flower inducing hormone, for root growth hormones provided by shoots, for a hormone that guides the pollen tube into the embryo sac where fertilization is accomplished, and for a senescence factor. It would abviously be simpler for us to interpret the result if such hormones do not prove to be varying hormones. (Salisbury, 1985. : 348-349)

Source : Sciencedirect.com

CHAPTER III CONCLUSION

1. Senescence mechanism is process of deterioration that accompany aging and lead to death of an organ or organism. 2. Pattern of senescence appear to differ in quite important ways, both in their causes and in the nature of the senescence processes, as well as in their degree of reversibility. 3. At cellular level, senescence appears to be tightly controlled, although the mechanism of control are not known. Senescing cells undergo reduction on their structure, and much of the membranous subcellular inclusions are disrupted. 4. Root do indeed produce cytokinin, and it has now become reasonably certain that the antisenescence hormone translocated from roots is in fact a cytokinin or a group of cytokinins. 5. Chemical analyses show that leaf senescence is accompanied by early losses in chlorophyll, RNA, and proteins, including many enzymes.

REFERENCES

Carl L. Wilson dkk.1962. Botany Third Edition.Usa :Holt, Rinchart and wintson Inc. Bidwell, R. G. S. 1979. Plant Physiology. New York: Macmillan Publishing Co., Inc.

Salisbury, Frank B. and Cleon W. Ross. 1985. Plant Physiology. California : Wardsworth Publishing Company