I know this is an older thread, but I was brought back here again by one of
@dw1305 's many links
I had another read through and there are some things which stick out to me 🤔
...
In the analysis of deficiency syndromes of plants it's important to realize where the limits of functionality are of individual elements. So for example, Deficiencies of the micronutrient metals should not result in structural degradation because they are not used to build structure and have no role in the maintenance of structure.
As far as I can see, this is downright wrong. Boron for example is very well known to play a huge role in plant structure, which is why terrestrial boron deficiencies often describe brittle plants, cracks and fissures and improperly formed structures as key symptoms.
All quotes following are from the book Marschner's Mineral Nutrition of Higher Plants (Third Edition 2012) unless otherwise noted.
..the primary role of B in the cell wall biosynthesis and structure results in a cascade of metabolic disruptions that can explain most, but not all, observed effects of B deficiency.
A role of B in cell wall structure has long been recognized. In B-deficient plants, the cell walls are strongly altered which is evident at macroscopic (e.g., ‘cracked stem’; ‘stem corkiness’; ‘hollow stem disorder’) and microscopic levels (Loomis and Durst, 1992; Shorrocks, 1997). Most anatomical deficiency symptoms are associated with cell wall abnormalities (Loomis and Durst, 1992; Brown et al., 2002) and the numerous biochemical and physiological effects often observed under B deficiency have been interpreted to be secondary effects of cell wall damage (Goldbach, 1997; Blevins and Lukaszewski, 1998; Brown et al., 2002; Bolanos et al., 2004).
The most prominent symptoms of B deficiency are associated with primary cell walls and include abnormally formed walls that are often thick, brittle, have altered mechanical properties and do not expand normally (Brown et al., 2002).
There are a lot more details but I dont think its necessary to quote the entire book.
A typical function of Manganese, for example is used in the enzymes that are responsible for splitting the water molecule into it's constituents parts, Hydrogen and Oxygen gasses. The release of Oxygen is the function of The Oxygen Evolving Complex (OEC) and this is where Mn is used in the hydrolysis. Other uses of this metal is as an activator of many enzymes used in the metabolism of organic acids as well as the assimilation of some macronutrients such as Nitrogen leading to chlorophyll production. So although a deficiency in Mn can look identical to an Fe shortage, i.e. discoloration, paleness etc., and can certainly negatively affect growth due to it's importance in photosynthesis and the subsequent reduction in carbohydrate production, in no way should it's absence affect structure or be involved in any kind of necrotic symptoms.
As X3NiTH has already partially pointed out, this is not entirely correct.
A role of Mn in nitrate reductase activity was presumed because of an increase in nitrate concentration in Mn-deficient leaves. However, this accumulation of nitrate is the consequence of a shortage of (i) reducing equivalents in the chloroplasts and (ii) carbohydrates in the cytoplasm, as well as of negative feedback regulation resulting from lower demand for reduced N in the new growth of deficient plants. There is no evidence of a direct role of Mn in nitrate reductase activity (Leidi and Gomes, 1985).
Inhibition of root growth in Mn-deficient plants is caused by shortage of carbohydrates as well as by a direct Mn requirement for growth (Campbell and Nable, 1988; Sadana et al., 2002). The rate of elongation appears to respond more rapidly to Mn deficiency than the rate of cell division. As shown in Fig. 7.10 with isolated tomato roots in sterile culture and an ample supply of carbohydrates (but without Mn), there was a decline in extension of the main axis in less than 2 days. Resupplying Mn rapidly restored the growth rate to normal levels if the deficiency was not too severe. In Mn-deficient plants, the formation of lateral roots ceased completely (Abbott, 1967). Compared to Mn-sufficient plants, there was a greater abundance of small non-vacuolated cells in Mn-deficient roots, indicating that Mn deficiency impairs cell elongation more strongly than cell division, an observation also supported by tissue culture experiments (Neumann and Steward, 1968).
The lower lignin concentration in Mn-deficient plants (Table 7.8) is a reflection of the requirement for Mn in various steps of lignin biosynthesis
Brief information about Lignin (since we have many members with english as their second language, myself included)
"Lignin is a class of complex organic polymers that form
key structural materials in the support tissues of most plants. Lignins are particularly important in the formation of cell walls, especially in wood and bark, because they lend rigidity and do not rot easily."
Another important example; Zinc is essential for plant growth because it controls the synthesis of a hormone called indoleacetic acid, which regulates plant growth. So, as with Mn, Zn is involve primarily with growth functions, not in structural issues and it's deficiency results in lower growth rate and chlorosis as opposed to necrosis. Deficiency also will show in new growth, not in mature leaves.
This is also partially incorrect
Zinc is required for maintenance of integrity of biomembranes.
Many of the most obvious symptoms of Zn deficiency such as leaf chlorosis and necrosis, inhibited shoot elongation and increased membrane permeability are expressions of oxidative stress brought about by higher generation of reactive oxygen species (ROS) and an impaired detoxification system in Zn-deficient plants.
The most characteristic visible symptoms of Zn deficiency in dicotyledonous plants are stunted growth due to shortening of internodes (‘rosetting’) and a drastic decrease in leaf size (‘little leaf’), as shown in Fig. 7.21. Under severe Zn deficiency, the shoot apices die (‘die-back’) as, for example, in forest plantations in South Australia (Boardman and McGuire, 1990). Quite often these symptoms are combined with chlorosis, which is either highly contrasting or diffusive (‘mottle leaf’).
In cereals such as wheat, typical symptoms are reduction in shoot elongation and development of whitish-brown necrotic patches on middle-aged leaves, whereas young leaves remain yellowish green in colour, but show no necrotic lesions (Cakmak et al., 1996a). Symptoms of chlorosis and necrosis in older leaves of Zn-deficient plants are often secondary effects caused by P or B toxicity, or by photooxidation resulting from impaired export of photosynthates.
I dont really see where the basis is for claiming that micronutrients are not used to build structure or have no role in it. They are clearly very involved in the process.
Perhaps I am misunderstanding the way you define "used to build structure" and "the maintenance of structure".
I also dont really understand how you can readily separate growth functions and structure building?
To have new structure you need growth, so if growth functions are impaired then the structure being made can be impaired too?