Homework assignment: read the below article, then in 2 short paragraphs: give me the strengths and in the 2nd paragraph the weakness of this theoretical treatment of hormones.
An Explanation of Plant Hormones
This theory replaces the article "A Start at a Comprehensive Theory of Plant Hormones." The old version is still available. Send comments to email@example.com.
In this article I will show, that if we make seven groups of assumptions about plant hormones, many of the most important questions of plant physiology can be answered. Auxin is seen here as made when there are good shoot growing conditions, that is when cells are receiving a good supply of shoot derived nutrients: sugar, CO2, and O2. Conversely gibberellin (GA) is seen as made under poor shoot conditions that is when sugar, CO2, and O2 are in short supply. Cytokinin is seen as made under good root conditions: a good supply of water and minerals. Conversely abscisic acid (ABA) is seen as made under bad root conditions: a scarcity of water and minerals. Ethylene, as is well accepted, is seen as made under overall stress conditions. Conversely, I add that brassinosteroid is made under good overall non-stressful conditions. Generally speaking I see plant hormones as being fully vital and integrated into growth, senescence, and nutrient transportation. I believe positive feedback loops are induced by auxin, cytokinin and brassinosteroid in immature cells under good growing conditions; that is, the better the nutrient conditions, the more of these hormones are made, causing more nutrients to be attracted to these immature cells, causing more hormones to be made etc. This effect is responsible for apical dominance in the shoot and root and works because mature cells make far less of these hormones than the immature cells. Hence nutrients are drawn away from the mature cells that produce them, to immature cells that need them to grow. This drainage does not complete to the point of senescence because the mature cells continue to make a small amount of protective auxin, cytokinin and/or brassinosteroid if the cells are still efficiently making or taking in nutrients. On the other hand, if a mature cell is not "pulling its own weight" nutrient-wise, that cell will start making GA, ABA, and/or ethylene. This will induce a positive feedback loop in the opposite direction, because these hormones push nutrients out of mature that cell (toward immature cells), and the more nutrients that are pushed out, the more of these negative hormones will be made. A vicious cycle is born, leading to senescence of inefficient mature cells and plant parts. Also in contrast to the positive hormones" (auxin, cytokinin and brassinosteroid), the negative hormones (GA, ABA, and or ethylene) are only made in small quantities in immature cells. This quantity is only enough to cause hibernation not senescence, so secondary buds, while not "profitable" nutrient-wise at a given time, are protected for possible future use.
This theory is designed to explain, in a simple way, the conditions under which hormones are made, how they are vital to nutrient transportation, how they induce apical dominance and senescence, the auxin-ethylene effect, and the hereto lack of totipotency found in many cultured calluses of plant species. Additionally, in response to criticism by Dr. Michael Jackson, some attempt is made to look at how plant hormones affect tissues, not just the conditions under which production occurs. Finally, I give a brief alternative theory, which comes from an original theory developed almost 12 years ago, which differs from the body of this work in some key ways.
I am not a professional scientist, although I have a BA in Biology from Swarthmore College and an MA in Biology from the University of Pennsylvania. My theory is speculative, though it builds on the work of others. Although I expect it to be, and it has already has been controversial, in defense of this theory it can serve as a starting point for future theories. This is the first broad theory of plant hormones that I am aware of. It can also serve to stimulate new experimentation, because of the novel concepts it contains. For example GA has not hereto been explicitly seen as a hormone that responds to sugar, CO2, and O2 deficiencies and ABA has not been seen as involved in mineral shortages.
Here is a more detailed and documented version of the theory described above with some additions not laid out in the Summary.
1. I believe Plant hormone production can be tied to abundance or scarcity of nutrients or good or bad conditions as follows:
* Auxin is made by all cells, to varying degrees, in response to a good supply of shoot-derived nutrients: light, sugar, CO2, and O2.
* Cytokinin is made by all cells, to varying degrees, in response to a good supply of root-derived nutrients: water and minerals.
* Brassinosteroid (BA) made by all cells, to varying degrees, under good overall, non-stressful growing conditions.
* Gibberellin (GA) is made by cells to varying degrees, facing a scarcity of shoot-derived nutrients: light, sugar, CO2, and O2.
* Abscisic Acid (ABA) is made by all cells, to varying degrees, facing a scarcity of root-derived nutrients: water and minerals.
* Ethylene is made by all cells, to varying degrees, faced with overall stress as is well known: weather, pest or disease.
From here on I will use the term positive hormones for those made under positive growing conditions: auxin, cytokinin, and brassinosteroid. I use the term negative hormones, as those made under negative growing conditions: GA, ABA, and ethylene. Positive and negative hormones are assumed to have largely opposite effects.
1. Research has shown that auxin is mainly made by young cells and drops as cells mature (Sembdner, et al., 1980). I speculate that all the positive hormones are made in large amounts in immature cells and drop off precipitously as cells mature. That is, faced with the same positive growing conditions, immature cells will make far greater amounts of positive hormones than mature cells.
I also speculate, that the negative hormones are made in small amounts in immature cells, and rise precipitously as the cells mature. That is, faced with the same negative conditions, a mature cell will make far more negative hormones than an immature cell.
2. Other research has shown that both auxin and cytokinin induce the uptake of all nutrients and hormones to their site of application (missing reference). I postulate that Brassinosteroid also has this effect. Coupled with the group of assumptions in point 1, this produces a runaway positive feedback loop. That is let's say, the shoot apical meristem is experiencing good growing conditions. It will then produce much auxin, because the shoot apex is immature tissue (see assumption 2). The cells' attraction of sugar, CO2, O2, minerals and water from surrounding tissue will induce even more auxin, cytokinin, and brassinosteroid (BA is made because of good growth conditions) production, and this will lead to an even greater uptake of nutrients and thus a positive feedback loop is created.
By analogy I also predict that the negative hormones push nutrients out of cells. This also induces a positive feedback loop in the opposite direction as the positive hormones, because a deprivation of nutrients particularly in mature cells leads to negative hormone production, which pushes out nutrients which in turn leads to a greater production of negative hormones. This should lead to senescence in mature cells but not immature ones, see below. Partial evidence is shown by the observation that ethylene leads the senescence of older leaves (Wareing and Phillips, 1981) as does ABA (reference missing).
3. I suggest that plant hormones affect the plant cells in three reversible stages according to their amounts. The first step involves activity in the cell. At low levels the positive hormones increase cell activity, whereas the negative hormones decrease, or induce suspension of activities.
Secondly, at intermediate levels, plant hormones affect cell dimensions. It has been documented that auxin, cytokinin, GA, ethylene, and brassinosteroid affect cell dimensions. My guess is that positive hormones increase average cell size in the plant overall, but tend to increase growth in the peripheral parts (leaves and outlying roots) faster than core parts of the plant (the stem and root core). Two of the negative hormones, GA (Engelke, et al., 1973) and ethylene (Burg and Burg, 1966) have been shown to cause increased cell size in some cells. However, I predict all three negative hormones cause a net shrinkage of cell size if averaged over the whole plant. GA for instance is a hormone concerned with shoot-derived nutrient deficiencies, thus GA may cause a shrinkage of less needed root cells. Certainly GA has been shown to stop root growth (Mitsuhashi-Kato, 1978). Along the same lines ABA is a hormone concerned with root-derived nutrient deficiencies. Perhaps then ABA causes shrinkage of less needed shoot cells.
Thirdly, at the highest levels, it has been shown that auxin and cytokinin are needed for cell division, I suggest that is also true for brassinosteroid. By analogy again, I also postulate that ethylene, ABA and GA are all three necessary for complete cell senescence.
4. Production of a small amount of a positive hormone in a mature cell can negate the effect of a large amount of negative hormones. This is already well known. A small amount of auxin for instance can prevent a leaf treated with ABA from going into senescence (reference missing). Conversely, it is possible that the production of a small amount of negative hormones in immature cells, perhaps in some cases, can negate treatment with a large amount of positive hormones.
I suggest that mature cells will make a small amount of life-saving positive hormones if the cell is still an efficient producer of nutrients. If the shoot cell is taking more than enough shoot derived materials to support both it and a sister root cell with their sugar, CO2, and O2 needs, than the cell is "profitable" and will make a small amount of auxin. If it is not making a "profit" of sugar, CO2, and O2, it starts making GA and also the other negative hormones. A similar schema, I would suggest, exists for root cells, cytokinin, and ABA, where cytokinin is made if enough minerals and water are taken in to support both the root cell and a cell of similar size or maturity in the shoot. If the root cell doesn't take in enough minerals and water, it makes ABA, and is excised.
5. I predict that positive hormones have the direct effect of inhibiting negative hormones and the indirect effect of promoting negative hormones and vice versa . For example the direct effect of auxin might be to inhibit ethylene production within the apical meristem, but the indirect effect is to draw nutrients from surrounding tissue inducing nutrient deprivation and thus stress and ethylene. If the ethylene then evolves up and comes into contact with the apical meristem directly, it directly inhibits auxin. This contrasts directly with the belief of most plant physiologists that auxin directly induces ethylene formation. I make this prediction in part to contrasts with the prevailing view so that the old belief will be reexamined. To view that positive hormones only directly inhibit negative ones is a simpler view and should be tested first. It is possible that positive hormones directly inhibit negative hormones when their are small amounts of positive hormones, but change to directly promoting negative hormones when their are large amounts of positive hormones. However again, this is a more complex view and it fails Occam's Razor for now.
6. I predict that the reaction of cells to negative hormones is context sensitive. For example if there is an excess of water (enough for growth) but a deficiency of minerals, the plant will still make ABA, but the cells will not react to this ABA in the fashion typically thought of. That is ABA is thought to be a water deficiency hormone and leaf cells will react by closing the guard cells. However in line with the above, I predict that ABA is still made in the face of good amounts of water, but in the face of deficiencies of minerals. The guard cells closing may be inappropriate under these conditions. Therefore the guard cells may remain open under high water and low mineral conditions. The reaction of cells to negative hormones may reflect the conditions within those cells rather than always exhibiting the reaction. In fact toxicity of nutrients, that is a level of nutrients that is detrimental to the plant such as too much water (flooding) and too much sugar may result in the release of negative hormones. The negative hormones would then not be just a signal of nutrient deficiencies but a signal of the overall health
Explanations and Predictions Arising from the Assumptions
* The major question that has been asked about plant hormones, is, what is their Function or why are they needed? I will go into detail about this below. However to sum up, I would say they allow the plant to respond in a balanced way to good or bad situations. For example let us say there are good shoot conditions and poor root conditions (e.g. plenty of light, but little water). This will produce auxin in greater overall amounts than cytokinin. As has been shown, this will lead to the induction of new roots (Torrey, 1957). I suspect the good shoot and poor root conditions also leads to an increase in ABA, which inhibits shoot growth (ABA's inhibition of shoot growth probably has been shown but I don't have the reference) and probably shifts energy towards the roots. This then leads to new supplies of root nutrients. This can be easily tested.
* Apical dominance looks to me like a simple case of the rich getting richer and the poor staying poor. The successful shoot apical meristem, by means of positive feedback multiplication eventually wins out in a war for nutrients. However since the secondary buds are only immature tissue, they do not make anywhere as near as much negative hormones to induce senescence, only enough to induce dormancy. Assumptions 1 & 3 would also explain the finding that both cytokinin and a mineral solution can break secondary bud inhibition. That is, the application of cytokinin to a secondary bud begins a new process of positive feedback for the bud where it attracts all of the nutrients and hormones it needs to allow it to grow (see assumption 3) and it induces the production of additional amounts of cytokinin in immature secondary bud cells once the minerals and water arrive (see assumption 1).
* Senescence is explained by the positive feedback loops for negative hormones mentioned in assumption 3 and the efficiency issues mentioned in assumption 5. That is, a newly shaded shoot cell, for example, that can no longer make enough sugar, and take in enough CO2, and O2, will start making GA (see assumption 5). The cell will first go into hibernation and the GA will cause the stem to lengthen perhaps bringing the leaf into better sunlight. If this allows the leaf to start making enough sugar, CO2, and O2, then the cell will start making auxin again and come out of hibernation.
If the stem lengthening induced by GA does not work, the GA will eventually start pushing nutrients out of the cell, inducing even more production of GA and some production of ABA and as well. This will cause stress to the cell inducing the production of ethylene. Now we have all three negative hormones pushing nutrients out of the cell, a real positive feedback loop, culminating in senescence. This is perhaps a simplistic model of what goes on, but I believe the general principle stands.
* Plant hormones have a big effect on nutrient transport. The positive hormones attract nutrients from the sites of harvesting or production in the mature cells, to the growing immature cells where the nutrients are needed. Auxin is transported downward from the apical meristem in the phloem. This suggests that auxin may be responsible for drawing sugar, CO2, and O2, from the leaves into the phloem for downward transport to the roots. The negative hormones also have the overall effect of pushing nutrients from inefficient mature cells toward efficient immature cells.
* The positive feedback loops produced by the positive hormones do not get carried away to the point of draining all the nutrients away from adjacent areas because of possibly three different mechanisms. First as mentioned above, auxin is transported down the stem so shoot nutrients don't just get attracted to the apical meristem, but to the entire phloem as the auxin is transported down in it. Cytokinin is transported in the xylem, and I would predict that water and minerals follow it up out of the roots and then up the stem, so root nutrients don't stay concentrated in the root apex.
Secondly as mentioned, a small amount of auxin produced by efficient mature plant parts protects it from the production of negative hormones. Thus mature parts are protected from complete draining because they never go into a negative hormone positive feedback loop. Thirdly it has been shown (reference missing) that some of the negative plant hormones may curtail the production directly of the positive hormones. This would be a negative feedback loop where the positive hormones induce nutrient deprivation in negative hormone producing tissue (non-efficient tissue), but the positive hormone levels are dampened, once the negative hormones reach a high enough level and travel back to the site of production of the positive hormones.
* The reason why secondary buds do not grow out, may not just be the simple reason that they only make a small amount of negative hormones, but may be a very dynamic process. For example the auxin production by the shoot apex induces the draining of nutrients from the secondary buds, inducing GA, ABA and Ethylene. Eventually these travel up to the shoot apex and directly inhibit the production of auxin. With a decrease in auxin their becomes a favorable cytokinin-auxin balance. Cytokinin is known to stimulate secondary bud growth. With the influx of nutrients to the secondary buds the negative hormones decrease precipitously, and the auxin production by the shoot apical meristem can start again. Thus the secondary buds may be poised between losing all their nutrients and dying off, or gaining nutrients and growing out and may be go through a periodic draining and refilling of nutrients to at least some extent.
* It has been shown that auxin is made in greater amounts in the shoot than in the root (Sembdner, et al., 1980). I would suggest this is because there is more sugar, CO2, and O2, in their point of origin, the shoot, than in the root. It has also been shown that more cytokinin is made in the root than in the shoot (Van Staden and Smith, 1978). I believe this is because there are more root-derived nutrients in the root than in the shoot. GA has been found more in the root than in the shoot (Barringtion, 1975) as one would expect, because there are less shoot derived nutrients there. Finally I would suggest that ABA is found in greater amounts in the shoot than the roots, because of the greater scarcity of water and minerals there.
* I predict that the positive hormones control the day life of the plant, since we can expect that they are made in greater concentrations in the day than the night. Auxin has been shown to peak during the day (Jahardhan, et al). Although Hewett and Wareing (1973) found cytokinin to peak once during the day and once at night not enough research has been done to show this conclusively for this effect to be thought to exist in an "average" plant.
Conversely the negative hormones rule the night, because we can expect with the lack of light and the decrease in temperature (slowing down nutrient harvesting machinery), less nutrients are brought in or created. Ethylene emanation from plants has been shown to decrease in the presence of light (Goeschl, et al., 1967). GA production has also been shown to go up in the dark and down in the light (Brown, et al., 1975). ABA has also been shown to peak at night (Lecoq, et al., 1983; McMichael and Hanny, 1977), although the latter only occurred under water stress.
Perhaps we may go so far as to predict that ABA and GA reverse the flow of nutrients at night. Possibly stores of sugar, CO2, and O2, found in the roots are hydrolyzed by GA and dumped into the xylem for shipment upward. Conversely maybe the flow of phloem is reversed at night to go from the roots or tubers to the shoot instead of the opposite direction. Again these things can be easily tested.
* Because of the direct and indirect influences hormones have on each other, we can expect that negative and positive hormones rise and fall in in contrasting waves. That is when positive hormones are high, then negative hormones are low, and when negative hormones are high positive hormones are low. Thus a plots of the amounts of negative and positive hormones should be two sinusoidal curves staggered by 180°. Although the biggest difference between the levels of positive and negative hormones should occur at the peak of the night and of the day, there should be a rise and fall of all hormones periodically during the whole night and day. Conceivably waves of hormones sweep through the plant as a kind of breathing many times a day.
* I suggest the quest for totipotency has been hindered because of the failure to recognize of the role of brassinosteroid. Possibly the success that has been had, is because some cell lines have a mutation allowing unprovoked native synthesis of brassinosteroid.
* Plants always respond to positive hormones by increasing activity or growing. They respond to negative hormones by becoming less active or smaller but stronger. Negative hormones cause downsizing.
* Auxin has been known to cause an increase in ethylene production upon application to tissues in high enough doses. My explanation of this comes from assumption 3. That is, auxin draws to it all kinds of nutrients from surrounding cells. This induces stress in surrounding tissue, thus causing ethylene production. I would guess that ABA and GA are also produced in these surrounding tissue. I would suspect the other two positive hormones produce same production of all the negative hormones.
Conversely the application of negative hormones should eventually cause an increase in positive hormones as measured in parts of the plant away from the site of application. This is because the negative hormones free up nutrients for use in other parts of the plant, which that stirs up a fresh wave of positive hormone production.
* It is possible that the effects of plant hormones are different according to which tissue they are in. For instance negative hormones may affect the peripheral parts differently than the core parts. I believe that the peripheral parts (the leaves and peripheral roots and tubers) first undergo hibernation, then cell shrinkage. Finally after the cell has undergone enough nutrient deprivation and stress and all the three hormones are present, senescence. On the other hand, I believe the core parts (the stem and root core) undergo first increased activity, then increased size and then cell division. In other words, in the presence of negative hormones the stem and the root core become stronger whereas the peripheral parts decrease in biomass. Again the plant becomes smaller but physically stronger under these environmental conditions. Also we can postulate that under the effect of negative hormones nutrients are stored in the core parts where they are less vulnerable. For example, under the influence of ABA, water is stored in a stem of increased girth so it will face less surface area and thereby evaporation.
Positive hormones may be the reverse of negative hormones in this respect. That resources may switched from less vulnerable core parts, outward to peripheral parts when the secure growing conditions signaled by the positive hormones are present.
An alternative to the theory above, would accept ABA as a water deficit signal alone (Wain, 1975), with nothing to do with minerals. Rearranging the above theory, brassinosteroid would be a water-abundance signal. Cytokinin could then be a signal of abundance of all nutrients, maybe (even including CO2, and O2), but excepting sugar. The part of this alternative theory that would be hard to swallow part would be that ethylene would have to take the role of a signal of all nutrient (excepting sugar) deficiency. Auxin and GA roles would then take roles of sugar abundance and sugar deficiency signal respectively. Seeing ethylene as a nutrient-deficiency hormone is difficult, since we are so accustomed to thinking of it as a stress hormone. However, clever experimentation could tease out this trait if it were true.
Many possible experiments could be done examining these ideas. The main theory may have possible weaknesses, for example, I am not aware that ABA has been tied to mineral deficiencies. Yet, the lack of supporting experiments may simply reflect the fact that scientists have not been looking at hormones in the light of way outlined here. I have come to believe that most Plant Physiologists are frustrated and do not believe an encompassing theory can be found. Thus they have not been looking for a theory. As ever though, "Seek and you shall find." (Matthew 7:7, Luke 11:9)
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