Plant hormones (idea) by socrtwo

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