Outline for a Comprehensive Theory of Plant Hormones
A prudent man keeps his knowledge to himself...A fool is only interested in airing his opinions.” Proverbs 12:23 and 18:2
In this Web page, I will discuss the functions, behavior and interrelationships of plant hormones. This is a further revision of the fourth and most recent version of my theories. The first version was written in 1986 and was not published or posted on the Web until recently. The second and third versions were written in 1995 and 1999. When the 1995 and 1999 versions were posted on the Internet, they attracted much comment, both positive and negative.
This paper sets out two alternative theories. The theories have elements in common but also differ fundamentally. The first theory is described in the more detail, with an introduction followed by a table of hormone characteristics. The section headed "Hormone Characteristics" includes additions that should be made to the table if the first theory is correct. Next, a section headed "Theory" sets out my basic understanding of why plant hormones are made and how they interrelate. Following this is a section headed "Predictions." This sets out the implications of the first theory. The final section of the paper is a summary of an alternative theory.
The first theory is that the five “classic” plant hormones, Auxin, Cytokinins (CKs), Gibberellins (GAs), Ethylene, and Abscisic Acid (ABA), plus the “new” plant hormones, Brassinosteroids (BAs), and Salicylates or Salicylic Acids (SAs) can be gathered into three groups. These are Growth Hormones, Stress Hormones and Shock Hormones. Auxin and CKs are Growth Hormones. Ethylene, GAs, and Brassinosteroids are Stress Hormones. And ABAs and SAs are Shock Hormones. All tree types of hormones are similar in that they fall within the classic definition of an intercellular hormone. They are made by a cell and are meant to affect the behavior of other cells, either in nearby tissue or at the opposite end of the plant.
The first assumption I make in both theories is that plants are interested in growing larger during the vegetative period of their life (the middle period, between germination and reproduction), and this growth requires both good environmental conditions and an amount of the four basic nutrient groups that exceeds that needed to keep the plant at its current size. The environmental conditions necessary for growth are optimal temperature, and the absence of environmental stresses, including high winds, pests, disease, and consumption by herbivores. The four basic nutrients required for growth are sugar, gases (Carbon Dioxide and Oxygen), water, and minerals. I generalize that Growth Hormones are made mostly in young and meristematic cells, and much less in mature cells. They are made in mature cells only when there is an excess of nutrients. I hypothesize that Stress Hormones, in contrast, are made in mature cells that are faced with a scarcity of nutrients and to a much lesser extent in young and meristematic cells faced with the same scarcity. The Shock Hormones differ from the other two groups in that they are made by all cells in equal amounts faced with the same conditions.
I suggest First they stimulate metabolism cause growth where cells have not reached physical maturity and its size limit. Second, they induce new growth (new shoots or roots from dormant shoot or root meristems) when active cells affected by the hormones have all reached their physical maturity and size limits. This really means the activation of dormant cells and the induction of growth in them. In both cases, growth is induced to use up the nutrient excess. Third, they induce new cell production through cell division when a balance of nutrients is available. I will explain more about this later on but this is real new growth and growth causation. When plant cells are dividing, I hypothesize that this usually means both the root and shoot are prospering and the plant is doing what it wants to do, mainly grow bigger. Fourth, Growth Hormones balance growth. If, for example, there is an excess of sugar and gases, the synthesized Growth Hormones will stimulate new growth or cell division in that part of the plant, for example the root, to balance out the excess of sugar and gases, with an excess of water and minerals. Fifth. they cause nutrient storage if growth is currently impossible or unwarranted. Sixth, if the plant is using more risky ways of obtaining nutrients (see below), they will make it switch to more conventional, less risky ways of obtaining them. I suggest that Auxin is made when the sugar and gases present in a cell exceed what is needed to support both it and any dependent cells at peak metabolic activity. I suggest that CK is made by the cell when the water and minerals present exceed what is needed to support both it and any dependent cells at peak metabolic activity. Auxin is found mostly in a young and meristematic shoots, but also by any cell with more sugar and gases than it needs for survival at the peak metabolic activity for both it and any dependent cell. Thus, Auxin will be made by young and mature roots, albeit in small amounts. One issue that needs to be cleared up in this scheme is whether growth hormones are ever released when cells are not at their peak metabolic activity. That is say the local cell environment is at high level of three out of the four required nutrients e.g. there is an excess of three out four nutrients, do growth hormones get released, but they trigger storage instead of growth?
Stress Hormones complement Growth Hormones. They are triggered by a deficit of nutrients that is when there are not enough nutrients to allow growth. The Stress Hormones do six things. First they cause the release of stored nutrients. Second, they inhibit growth. Third, they cause the senescence of older plant parts in that part of the plant. So, if an older leaf or root cell does not have more the minerals and water necessary for the cell and any dependent cells to survive at peak metabolic activity, it will make Stress Hormones. The Stress Hormones then inhibit the growth of the shoot and cause the senescence of older, less efficient leaves, which have no part in making up the water and mineral deficit, except in the short term by releasing their cell contents of water and minerals in a one-off burst of senescence. This growth inhibition and senescence of older, less efficient leaves both stops the deficit from worsening and actually reverses it. This reversal occurs beyond the short-term release of water and minerals originally used in the dying cell’s biological structure, because there are now fewer leaves needing water and minerals. There is now less of a biomass needing support with these nutrients. The fourth thing that a Stress Hormone does to make up these deficits is exaggerate the rate of growth of the part of the plant that normally procures the nutrient. Thus the Stress Hormone in this case would exaggerate root growth. The fifth thing a Stress Hormone does is change the nutrient procurement strategy and to use more risky strategies. For instance, the Stress Hormone synthesized by mineral and water stresses induces the growth of root hairs in the root, which greatly increases the surface area of the root and water and mineral absorption, but may make the plant more susceptible to water loss during rapidly developing drought conditions, to disease or to pestilence. The root hairs are behind the thick waxy protective cuticle of the root. As many of you will have guessed by now, I am assigning Ethylene to this role of mineral and water nutrient deficit indicator. I assign GAs as indicators of sugar and gas deficits. I will also argue later that in fact the release of Stress Hormones is a normal part of the life of the plant, at least at night, because active procurement of nutrients is much harder during this period. This leads to the sixth feature of stress hormones, that they too balance growth proportions of cells. Ethylene broadens plant cells and GA lengthens them, so at night when both these hormones are high and Auxin and CK are low, cell proportions are still balanced.
Finally we come to the Shock Hormones. I group ABAs and SAs here. It is widely accepted that ABA is rapidly released when a plant confronts stress of most kinds. It is beginning to become accepted SA is released when a plant obtains release from these survival threats. It’s not much of a stretch to see ABA as putting the plant in a defensive posture of dormancy and maximum self protection. SA would then open the plant back to normal functioning after the threat is gone. I would see all cells making ABA in similar amounts when confronted with the same stress. The same would be true of SA. Perhaps only beyond peak rates of metabolism would the Growth Hormones Cytokinin and Auxin be released. A climactic rise or sustained high level of SA may be the signal that a plant has reached this point and that resources beyond this can be turned to Growth. On the low end, a climactic or sustained high level of ABA maybe necessary prerequisite to the synthesis of GA and Ethylene in that it would be a signal that the levels of nutrients has dipped below survivable levels.
The alternative theory says that instead of Auxin and Cytokinin being released when there are more than enough nutrients for peak level metabolism, they are instead released any time nutrients get above survivable levels. Also the second theory would say that GA and Ethylene would be released any time nutrients fall below peak metabolism rates. Therefore an absence of GA and Ethylene and the presence of high levels of Cytokinin and Auxin would be a signal of passing of peak metabolism conditions and conditions warranting growth. On the low end, the presence of high levels of GA and Ethylene and the absence of Auxin and Cytokinin would be an indication that senescence is warranted and survivable levels of nutrients are not indicated. In this scheme, ABA and SA would fall to the role of a plant’s responses to rapidly developing stress or release from such a threat. SA would be used to release a plant from a defensive dormant posture. This is the way most plant scientists see ABA anyway and are beginning to see SA’s role.
Finally this theory has its limitation. Brassinosteroid is accepted by some but by no means all Plant Physiologists as being part or the primary hormone induced in the GA hormone cascade. I don’t enter this discussion except to provisionally accept that this is true. On the subject of Jasmonates, I won’t say much except that it seems obvious to me that they are induced by wounding and help coordinate the plant’s defenses to counteract such an event. This is a special case of plant stress and will not be discussed here except to say that it induces ABA as part of its process, and when ABA is induced it falls under the purview of this general theory. This theory attempts to provide a backbone or generalized framework from which to understand plant hormone behavior. Despite Galston’s great work, I too will not include a discussion of polyamines as it is still unclear as to whether these chemicals are hormones or are membrane stabilizer released by hormones under stress conditions.
Introduction
Since Darwin’s time, it has been known that plants regulate their growth with some kind of internally secreted chemicals. Plant hormones, according to a standard definition from the Web:
Are signal molecules produced at specific locations;
Occur in low concentrations;
Cause altered processes in target cells at other locations.
Today, it is accepted that there are five major classes of plant hormones, with a few possible candidates to add in the future. The five major classes are Auxin, CKs, Ethylene, GAs, and ABA. Recently it has been suggested that BAs, JAs, SAs, and Polyamines are new major classes of hormones. This paper is not an introduction to the discovery, chemical structure, and synthesis pathways of the hormones. There are several decent introductions to these on the Web. Instead, I shall try to provide a second-level examination of the hormones and a unifying outline of a theory that explains the underlying relationships and generalized principles under when these hormones are secreted. This paper is a simplification of the findings. I want to warn any reader, that I have a strong preference for symmetry in theories and models. Inspired by the fact that plants show a strong physical symmetry, being divided into roots and shoots, my two theories will each be strongly symmetrical.
Any theory of plant hormones needs to recognize the work of K. V. Thimann, F. Went, F. Abeles, F. Skoog, G. Avery, P. F. Wareing, P. Davies, P. W. Morgan, W. P. Jacobs, A. C. Leopold, A. W. Galston, R. Cleland, and F. Addicott. Forgive me for leaving out the names of countless others who have made major contributions to the field. Special thanks go to Mark Jacobs for getting me so interested in plants in the first place.
Hormone Characteristics Table
All items in bold are known scientific findings - references are in progress
All items with “?” within parenthesis "( )" are from papers known
from my research notes whose dates I did not record
All items with “?” not within parenthesis, present difficulties to the theory outlined below
All items in italics, are speculations on my part
In this table, the name of hormone with a chemical example of the class is followed by location,
characteristics and occasions for synthesis induction and this is followed by effects of release and treatment
Auxins- IAA
- Location and Characteristics of Synthesis -
Synthesized in shoot and root meristematic tissue (Sembdner et al., 1980)
Synthesized in young leaves (Sembdner et al., 1980)
Synthesized in mature leaves in very small amounts
IAA peaks during the day (Jahardhan et al., 1973)
Synthesized in mature root cells
Released by meristematic cells when they have enough sugar and Oxygen to support both themselves and any dependent cells and are in good growing conditions
Released by all cells when they are experiencing conditions which would normally cause a shoot meristematic cell to produce Auxin
Directly or indirectly induced by high levels of Ethylene
- Effects of release and treatment -
Stimulates cell elongation (Schneider, 1938)
Stimulates cell division with CK
Induces xylem and phloem (Jacobs, 1967)
Directly stimulates Ethylene synthesis
IAA inhibits Ethylene formation and transport of precursor (Wright, 1980)
Induces shoot apical dominance (Snow, 1945; Palmer & Phillips, 1963)
Inhibits abscission prior to formation of abscission layer (inhibits senescence of leaves)
Involved in phototropism, gravitropism, tropism toward moisture
Induces sugar and mineral accumulation at the site of application (Mitchell et al., 1937; Booth, ?; Davis and Wareing, ? )
Flower initiation
Sex determination
Induces xylem and phloem
Induces new root formation (Torrey, 1957; Brown et al., 1975) by breaking root apical dominance induced by CK
Inhibits root hair growth and causes them to die back
(From Theory II) Stimulates the rate of metabolism of cells in the root (who are not at their peak metabolism rates) in response to an increase in the levels sugar and essential gases
Cytokinins (CKs) - Zeatin
- Location and Characteristics of Synthesis -
Synthesized in root and shoot meristematic tissue (Chen et al., 1985)
Synthesized in meristematic regions of roots (van Staden & Smith, 1978)
Synthesized in mature roots – small amount
Rapid transport in xylem stream
CK activity reduced in plants suffering drought (Vaadia, 1965)
Peaks during the day (Hewett & Wareing, 1973)
Synthesized in mature shoot cells
Released by meristematic cells when they have enough minerals and water to support both themselves and any dependent cells
Released by all cells when they are experiencing conditions which would normally cause a shoot meristematic cell to produce CK
Directly or indirectly induced by high levels of GA/BA
- Effects of release and treatment -
CK promotes Chlorophyll production and leaf unrolling (Beevers et al., 1970)
CK promotes photosynthesis (Adedipe et al., 1979)
Stimulates cell broadening (Egelke et al., 1973)
Also promotes shoot formation (Skoog & Miller, 1957)
Also promotes the unloading of sugar from phloem (Hayes & Patrick, 1985)
Causes the outgrowth of secondary shoot buds – breaks shoot apical dominance/ lateral bud development (Sachs & Thimann, 1967)
Delays leaf senescence (Pooviah & Leopold, 1973)
Stimulates cell division with Auxin
Involved in morphogenesis (Houck & Lamotte, 1977)
Promotes stomatal opening
Induces xylem and phloem
Directly induces GA/BA at high levels
Inhibits C4 Photosynthesis
(From Theory II) Stimulates the rate of metabolism of cells in the shoot (who are not at their peak metabolism rates) in response to an increase in the levels minerals and water
Ethylene (ET) - Ethylene
- Location and Characteristics of Synthesis -
Directly induced by high levels of Auxin (Rubinstein & Leopold, 1964)
Found in germinating seeds (Esashi & Leopold, 1970)
Induced by root flooding (Kawase, 1972; El-Beltagy et al., 1974; Imaseki, 1985)
Induced by drought (El-Beltagy et al., 1974)
Synthesized in nodes of stems
Synthesized in tissues of ripening fruits
Synthesized in response to shoot environmental, pest, or disease stress
Synthesized in senescent leaves and flowers
Rapidly diffuses
Inhibiting effects of Ethylene on shoot growth (more specifically on stem elongation) reduced in the presence of light (Wareing & Phillips, 1981). Also Ethylene levels are decreased by light (Goeschl et al., 1967)
Released in mature cells when they do not have enough minerals and water to support both themselves and any dependent cells
Released by all cells when they are experiencing conditions which would normally cause a mature shoot cell to produce Ethylene
- Effects of release and treatment -
Stimulates leaf and flower senescence (Wareing & Phillips, 1981)
Induces leaf abscission (El-Beltagy et al., 1974) mainly in older versus younger leaves (Leopold, 1970)
Induces seed germination (Esashi & Leopold, 1969; Ketring & Morgan, 1970)
Induces root hair growth – this increases the efficiency of water and mineral absorption
Stimulates Epinasty – leaf petiole grows out, leaf hangs down and curls into itself
Stimulates fruit ripening
Induces the growth of adventitious roots during flooding
Usually inhibits growth (El-Beltagy et al., 1974) - just shoot growth
Affects neighboring individuals
Disease/wounding resistance
Triple response when applied to seedlings – root ? and shoot growth inhibition and pronounced hypocotyl hook bending
Inhibits stem swelling ? (Contradictory to the finding below – contradictory sources)
Stimulates cell broadening (Burg & Burg, 1966) (and lateral root growth)
Interference with Auxin transport (when hormone levels are increasing)
Directly or indirectly induces Auxin at high levels
(From Theory II) Inhibits the rate of metabolism of cells in the shoot (who are not already at their lowest metabolism rates) in response to an decrease in the levels minerals and/or water
Gibberellins (GAs) - Gibberellin 452D
- Location and Characteristics of Synthesis -
Synthesized in the embryo (Webb et al., 1973) and germinating seeds
Synthesized in the roots (Barrington, 1975)
Levels go up in the dark when sugar cannot be manufactured and down in the light (Brown et al, 1975)
Synthesized in apical meristems ? and young leaves ?
Produced in the stem rather than the growing tip ? (opposite finding to above – conflicting sources)
Transport is non-polar, bidirectional producing general responses
Released in mature cells (particularly root) when they do not have enough sugar and Oxygen to support both themselves and any dependent cell
Released by all cells when they are experiencing conditions which would normally cause a mature root cell to produce GA or BA
Released in response to root environmental, pest, or disease stress
Directly induced by high levels of CK
- Effects of release and treatment -
Stimulates shoot and cell elongation (Engelke et al, 1973)
Delays senescence of leaves (Manos & Goldthwaite, 1975; Goldthwaite, 1972)
Inhibits root growth (Thimann, 1977; Mitsuhashi-Kato et al., 1978)
Inhibits adventitious root growth (Rossel ?)
Produces seed germination (Egley, 1980)
Antagonist promotes root growth and GA reverses this (Kefford, ?)
Promotes root initiation in low concentration in pea cuttings (Eriksen, 1970, 1971)
Stimulates bolting and flowering in biennials (Zeevaart, 1983)
Regulates production of hydrolytic enzymes for digesting starches (Varner, 1964)
Inhibits CK bud growth on calluses (Engelke et al., 1973)
Inhibits bud formation (Murashige, 1964)
Inhibits leaf formation (Bryan et al., 1955; Tronchet, 1968)
Breaking of dormancy
Induces extra Chlorophyll production or more efficient methods of photosynthesis (C4Photsynthesis). I think this reference actually exists
Stimulates root senescence
Directly or indirectly induces CK at high levels
(From Theory II) Inhibits the rate of metabolism of cells in the roots (who are not already at their lowest metabolism rates) in response to an decrease in the levels sugar and/or essential gases
Abscisic Acid (ABA) - Abscisic Acid
- Location and Characteristics of Synthesis -
Released during desiccation (Wain, 1975)
Has been found to peak at night (Lecoq et al., 1983 a, b)
Synthesized in green fruit and seeds at the beginning of the wintering period
As well as moving within the leaf it can be transferred to the leaf from the roots by the transpiration stream
Rapidly translocated
Produced in response to stress
Synthesized in leaves and stems (particularly when water stressed)
Released by cells in danger of not having enough nutrients locally or good enough environmental conditions to survive
All cells capable of synthesizing
- Effects of release and treatment -
Stimulates stomatal closure (Wain 1975)
Fruit ripening inhibition
Encourages seed dormancy by inhibiting cell growth – inhibits seed germination
ABA inhibits the uptake of Kinetin (Reed, 1974)
Pathogen resistance response defense -
Induces senescence in already damaged cells and their proximate neighbors
Quickly puts a plant, organ, tissue or individual cell in a defensive posture (whatever this entails) in response to rapidly developing nutrient or environmental stress that threaten their survival
Decreases metabolism in response to a newly developing deficiency of nutrient or adverse environmental condition, such that condition becomes survivable at the new lower level of metabolism (Not true in Theory II)
Possibly induces cell dormancy or senescence by a climactic increase or sustained level stimulating the synthesis of GA and/or Ethylene (Not true in Theory II)
A climactic rise or sustained level of ABA may be a prerequisite for the synthesis of any GA and/or Ethylene in that it presence indicates unusable or unsurvivable levels of Water, Sugar, Minerals and/or essential gases (Not true in Theory II
Brassinosteroids (BAs) - Brassinolid
- Location and Characteristics of Synthesis -
Released in mature cells when they have less than enough sugar and Oxygen to support both themselves and any dependent cells
Released by all cells when they are experiencing conditions which would normally cause a mature root cell to produce BA or GA
Released in response to root environmental, pest, or disease stress
- Effects of release and treatment -
Increased rate of stem elongation (Thompson et al., 1982)
Leaf senescence inhibition
Involved in gravitropism
Bending of grass leaves at the sheath/blade joints
Inhibits leaf abscission
Inhibits root growth
Resistance to stress - just in the shoot. By rerouting resources from the root to the stressed shoot
Stimulates cell elongation and division (Thompson et al., 1982) – just in the shoot
Enhanced Ethylene production ? – induced indirectly by the causation of root cell senescence
Promotion of growth - just shoot growth
Xylem differentiation promotion - in order to transfer resources from cannibalized root cells
(From Theory II): inhibits the rate of metabolism of cells in the shoot (who are not already at their lowest metabolism rates) in response to an decrease in the levels sugar and/or essential gases
Jasmonates (JAs) - Jasmonic Acid
- Location and Characteristics of Synthesis -
Desiccation
Effect of elevated ABA levels
JA-induced proteins are lacking in the roots, in bleached leaves, and in leaves of chlorophyll-deficient
- Effects of release and treatment -
Growth inhibition
Senescence promotion
Stimulates wound responses
Germination inhibition
Tuber formation promotion
Fruit ripening and fruit abscission promotion
Pigment formation promotion
May have a role in plant defense
Salicylates (SAs) - Salicylic Acid
- Location and Characteristics of Synthesis -
Cells returning from water stress
Released by cells secure in having more than enough nutrients and environmental conditions locally to survive at its current metabolic level
All cells capable of synthesizing
Has its effect or acts by rapid local increases followed by rapid decreases in levels
- Effects of release and treatment -
Retards senescence (regulatory role) – probably by inhibiting Ethylene biosynthesis
Induces flowering
Inhibits seed germination – by inhibiting ABA synthesis
May also block the wound response and act antagonistically to ABA – preventing the wound response from spreading further than necessary
After a survival threat has passed SA quickly removes a plant, organ, tissue or cell from a defensive posture and returns it to normal functioning
Increases cell metabolism rate to take advantage of new complete more advantageous nutrient and environmental conditions (Not true in Theory II)
A climactic or sustained level of SA may occur if a cell has reached its peak metabolic levels and may signal that a plant’s resources can be turned to growth (Not true in Theory II)
This climactic or sustained level of SA may be a prerequisite for the synthesis of Auxin and/or Cytokinin, because only then does a plant know that it has enough resources to turn them to growing bigger (Not true in Theory II)
Information provided initially by: (some of the links are dead, so I am giving you the Internet Archive index pages of the sites to find them. Some were just not archived by that system so may be dead to the world). archived link of http://www.sidwell.edu/sidwell.resources/bio/VirtualLB/plant/hormone.html, dead link of http://www.psc.ttu.edu/ps3323/PPT%20Files/HORMONES.ppt, live link of http://www.biologie.uni-hamburg.de/b-online/e31/31f.htm, live link of http://styx.nsci.plu.edu/~dhansen/hormones2.ppt, dead link of http://www.pasionflow.co.uk/horm.htm, live link of http://www.umanitoba.ca/faculties/afs/plant_science/courses/39_768/l18/l18.1.html and archived link of http://www.nslc.wustl.edu/courses/Bio4021/2003/L18.htm.
Theory
1. The goal of a plant is to germinate, survive, grow, and reproduce (and either exploit or contribute to life in general – see my summary of a future paper in progress here).
2. The role of the shoot is to create sugars from sunlight, water, and Carbon Dioxide harvested from the air. It also harvests most of the Oxygen needed by the plant for respiration. The shoot may serve as a reserve store for water and minerals. This may be far fetched as a general principle but the storage of water occurs in at least the cactus. The best place for storing all nutrients may be out of harms way in the soil, in the root. The shoot also provides the structure that supports the leaves, flowers, and fruit, but this will not be important here.
3. The role of the root is to harvest water and minerals from the soil. In order to function, the root also needs to harvest some Oxygen from spaces between the soil particles. The root also provides a place for storing reserves of sugar in the form of starch and may even store Oxygen. It also anchors the plant in a propitious place for it to grow and prevents it from being physically uprooted by the elements or fauna. The anchoring role of the root will not be important here.
4. If they