Addendum

There are a two alternatives that I can imagine to the most important issue of what triggers the synthesis of Growth and Stress Hormones.

The first alternative trigger for Auxin and Cytokinin any time nutrients go above survivable levels (and there are good environmental conditions).  Contrast this with the main theory that says growth hormones are released when the cell has more than enough nutrients to exist at peak metabolic levels.  Auxin is then stimulated by above survivable levels of sugar and essential gases.   Cytokinin is then stimulated by above survivable levels of minerals and water.  Auxin and Cytokinin being signals of nutrients levels, might then stimulate their use by increasing the speed of metabolism or inducing growth and cell division.

Similarly, GA and Ethylene could released when nutrients fall below that which is needed for peak metabolism.  GA could be released when sugar and essential gases fall below the level needed for peak metabolism.  Ethylene could be released when minerals and water fall below this peak level.  GA and Ethylene might then work by doing their best to attempt to address the shortfall by decreasing the speed of metabolism, inducing cell dormancy and inducing senescence.

In this second scheme whenever nutrient levels fall between peak metabolism and survivable nutrient levels, we can expect both Stress and Growth Hormones to be synthesized.  Since shoots are the organs that make sugar and harvest essential gases, we can expect that those levels would rarely fall below peak metabolism nutrient levels.  Thus we can expect that Gibberellin is rarely synthesized in the shoot.  I know there is supposedly experimental evidence that this is untrue, but perhaps it should be looked at again more closely.  This is not to say that GA is not found in the shoot.  From the definition of a hormone we can expect that the effect of a hormone occurs at a distant location from its synthesis. I would expect GA to be mostly made in the root where sugar and essential gases often fall below peak metabolism levels.  Synthesis may occur in the roots, but the effects GA has are in the shoot as well as the root.  As in the first version of theory, I believe all of GA’s effects are meant to address shortfalls in sugar and essential gases.  This would include root growth inhibition and senescence, shoot lengthening, shoot preservation from senescence, and the changing of photosynthesis to a more efficient but more risky method.

Also complimentarily, we can expect Ethylene to be rarely synthesized in the root, where levels of minerals and water seldom fall below those needed for peak metabolism.  This is not to say that similar to GA and the shoot, that Ethylene does not have a big effect on roots.  Again just like in the first theory, I believe everything Ethylene does is to address nonideal levels of minerals and water.  Thus Ethylene inhibits shoot and leaf growth, induces leaf senescence, initiates the somewhat risky growth of root hairs, preserves roots from senescence and causes roots to branch out and to make new lateral growth in the soil. 

In this second scheme we can also postulate an explanation for cell dormancy like the dormancy that exists in secondary buds.  That would be that perhaps at low levels GA and Ethylene would attract all nutrients instead of pushing them out.  On the other side, perhaps at low levels Auxin and Cytokinin would push nutrients out of a cell.  Thus a dynamic yet stable equilibrium would exist at very low levels of nutrients.  The movement into real metabolism or back toward senescence would need amounts or deficiencies in nutrients beyond which caused the synthesis of GA and Ethylene acting in their nutrient attraction mode, and Auxin and Cytokinin acting in their nutrient pushing mode.  Enough nutrients would need to be around to push a cell out of a stable valley of minimum metabolism.  Perhaps another similar equilibrium exists at the peak metabolism point.

A third scheme could be envisioned where Growth Hormones are made whenever an increase in nutrients is detected at all from previous conditions.  In this case the first role of the hormone would be as a metabolism stimulator.  This would produce negative feedback so that the excess nutrients are used up by a higher level of metabolism stimulated by the hormones.  A steadily increasing level of the hormones might then be an indication to the plant that peak metabolism has been reached so the cells have nowhere to go metabolism wise, no negative feedback occurs and growth is now warranted.

A similar scheme question could also be addressed about Stress Hormones.  That is are stress hormones released only when plant cells fall below the minimum level of nutrients necessary for survival or do they follow any decrease from previous levels.  In the latter case the first role of Stress Hormones would be to decrease the rate of metabolism.