16.3.4  Diagnosis of deficiencies

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Almost all Australian soils are low in one or more available nutrients, sometimes dominating the distribution of native flora and severely limiting crop and pasture production. Diagnosis of nutrient deficiencies in plants and prognosis of likely nutrient deficiencies in a forthcoming growing season are fundamental to agricultural production and ecosystem management.

One standard procedure for defining those nutrients likely to be deficient in a soil for crop growth is to apply fertiliser trials to crops on representative soil types in the field or in pots. Soil analyses are also useful for some nutrients. Visible symptoms often act as useful guides to nutrient deficiencies especially when interpreted in relation to nutrient function and mobility within a plant. They are sometimes sufficiently specific for definitive diagnosis, as, for example, with split seed in Mn-deficient lupins. Visible symptoms have been especially useful in development of Australian agriculture but they can be too general for diagnosis and may be confused with symptoms of other stresses. For example, both frost and Cu deficiency at flowering can produce identical empty heads of wheat at maturity. In the absence of leaf symptoms, an underlying Cu deficiency will not have been detected until too late, and yield will have already been severely depressed.

One convenient method for assessing soil–plant nutrient status is to analyse total nutrient concentrations in dried plant material. Figure 16.5 shows an ideal relationship of nutrient concentration to plant growth for such diagnosis. Nutrient concentrations below a minimum or ‘critical’ concentration indicate that nutrient deficiency is restricting plant growth; concentrations above another ‘critical’ concentration are toxic; concentrations between the two critical values signify adequate to luxury nutrient status.


Figure 16.7 An anomalous relationship between plant growth and Cu concentration in whole tops of barley plants, showing a 'Piper-Steenbjerg' effect brought on by severe Cu deficiency where dry mass in leaf blades increases relative to that in stems plus petioles which also retain higher Cu concentrations than leaves. The net outcome of this partitioning in dry matter and Cu between leaf blades and petioles plus stems is a higher Cu concentration in shoots with sever deficiency than in shoots with only marginal deficiency (Based on Steenbjerg 1951; see also Smith and Loneragan 1997)

Nutrient concentrations in whole-plant shoots have often proved unsatisfactory for several reasons including change in critical values with plant age and low mobility of some nutrients from old leaves to growing regions. In extreme cases, nutrient concentration of severely deficient plants may be higher than that of healthy plants, giving a C-shaped curve commonly known as the ‘Piper–Steenbjerg’ effect, after the first scientists to record it (Figure 16.7). Concentrations in specific plant parts of similar physiological age such as most recently expanded leaf blades in cereals generally give more instructive relationships.

Physiological activities, metabolite concentrations, physical measurements such as in vivo chlorophyll a fluorescence for Mn deficiency (Figure 16.3) and leaf absorption or reflectance of light for N deficiency have all been used as the basis of other diagnostic tests. In addition, enzyme activities and con-cen-trations or ratios of all or selected forms of nutrients in living and dead plant parts and expressed sap find application. Given a clear understanding of nutrient function, physiological tools are excellent for diagnosing individual nutrient deficiencies.

From measurements during growth, diagnostic tests have also been used as prognostic tests which predict the likely impact of nutrient deficiencies at harvest. Such predictions need additional information on the ability of soils to supply nutrients and the size of remobilisable reserves within plants. They must also estimate the likely environmental conditions between sampling and harvest, and for this reason are only indicative. Where sufficient data are available, this information has been incorporated into static and dynamic simulation models which predict the likely value of fertiliser applications and hence provide a firm basis for fertiliser recommendations.

(a)  Deficiencies of group 1 nutrients: N, S

As nitrogen and sulphur are essential components of all the structural and metabolic proteins in plants, they influence all processes of growth and metabolism. For both nutrients the first visible symptom of deficiency is the paling of the green colour of leaves due to their low chlorophyll concentration.

Paling develops first in old leaves of N-deficient plants while young and developing leaves remain green. Paling spreads to younger leaves as the deficiency intensifies. This charac-teristic pattern results from an effect of N deficiency in initiating senescence of older leaves and the export from them of metabolites from the breakdown of their proteins and chlorophyll to younger organs.

While the symptoms of sulphur deficiency also result from loss of chlorophyll from leaves, the pattern of the resulting paleness and yellowing vary with N supply. In legumes dependent on symbiotic fixation of their N supply, the symptoms of S deficiency are identical with those of N deficiency in plants without an effective symbiosis. In non-leguminous plants with a low level of N supply, the symptoms of S-deficiency may also resemble those of N deficiency. But in plants with adequate N, the onset of S-deficiency does not induce senescence in old leaves so that they remain green in S-deficient plants while the young leaves become pale and yellow from failure of chlorophyll synthesis.

Paling and yellowing of old leaves occurs in N- and S-deficient plants, and is often associated with development of reddish colours in petioles and leaves resulting from accumu-lation of anthocyanin pigments. Old leaves of S-deficient plants remain green, while young leaves are generally bright yellow rather than reddish.

Sulphur deficiency was not a problem for most Australian crops and pastures while single superphosphate, which contains over 11% S, was the main source of P fertilisers. Following introduction and expanding use of high-P fertilisers with lower S contents, S deficiency has become more important, especially in pastures.

In soils, inorganic S occurs almost entirely as sulphate, which is much less strongly adsorbed than phosphate. Indeed, for many soils in higher rainfall regions, fertiliser S is readily leached so that autumn applications are lost well ahead of the following spring.

Organic S in soils is closely associated with C and N of organic matter at a level of about 10% of the N content. Mineralisation of soil organic matter in cropping generally supplied sufficient S for crop growth unless fertiliser N is applied. Accumulation of soil organic matter by pastures generally exceeds mineralisation, so that S deficiency is more common with pastures than with crops.

(b)  Deficiencies of group 2 nutrients: P, B


Like N deficiency, P deficiency often enhances anthocyanin production, producing red or purple colours in plant stems, petioles and leaves. P differs from N deficiency in that leaves have a darker green colour due to a high chlorophyll concen-tration which in turn results from P deficiency depressing cell expansion more strongly than chlorophyll production. P deficiency disturbs most metabolic processes and particularly photosynthesis and carbohydrate metabolism.

Ecologists have found P to be the main nutrient limiting growth of several Australian native plant communities and have suggesed that soil P influences community boundaries and floristic composition. Native soil P has also been almost universally deficient for agricultural production, and especially P-fixing soils such as red-brown earths (oxisols in Table 16.1). Black earths of southeastern Queensland and northern New South Wales (vertisols in Table 16.1) are a notable exception to this chronic P deficiency. Crops have been grown there for over 90 years without P fertilisers, and in small areas of soils in a few other localities P has been adequate.

Many million tonnes of phosphatic fertilisers have now been put on Australian crops and pastures. In all soils except siliceous sands from which it leaches, fertiliser P reacts strongly with Ca, Fe and Al minerals (P sorption in Table 16.1), making a large proportion unavailable to plants. Organic P compounds which accumulate under pastures in most soils tie up additional fertiliser P, and until such soil reactions reach equilibrium P has to be added in excess of immediate plant requirements to ensure maximum plant yield. With continued application of excess P fertiliser, plant-available P in soils eventually reaches a level where maximum yield can be maintained by dressings equal to the amount removed in agricultural produce. Pastures on many soils need around 150–200 kg P ha–1 to reach that point. Cereals on similar soils need 200–250 kg P ha–1 to offset losses due to mixing of fertiliser P through a larger volume of soil compared with surface application to pastures. Such applications represent a substantial cost to farmers, and crops on about half of Australia’s agricultural soils remain undernourished with respect to P nutrition.

In terms of soil–plant dynamics, fertiliser P that appears to be rendered unavailable by soil reactions is in fact still acces-sible to plants, but in a protracted fashion. Native ecosystems that operate at a slow tempo have adapted to this inertial release via specialised roots and associations with microorganisms (Sections 3.6, 16.4), but in agricultural environments, soil P is released too slowly to meet internal P requirement for maximum yield of present-day crop and pasture plants. A major challenge in this area for plant physiologists, breeders and genetic engineers is to develop plant cultivars with greater efficiency in extracting P from soils. Such cultivars would lower requirements for fertiliser P by enhancing access to ‘unavailable’ soil P reserves.


B deficiency symptoms sometimes appear as an interveinal chlorosis of young or recently matured leaves which may be confused with symptoms of other deficiencies. Other symptoms are sufficiently characteristic to provide a strong indication and even a definitive diagnosis of the deficiency. Charac-teristic symptoms include death and discolouration of apical meristems with consequent thickening of stems and multiple shooting of axillary buds; thickening of roots with multiple lateral apices close to the tip; and death and discolouration of internal tissues as in hollow heart of peanut kernels, heart rot of sugar beet and internal cork of apples.

Analogous to symptoms of B deficiency, symptoms of B toxicity also commonly occur as an interveinal chlorosis, but they develop first on old leaves and the pattern of chlorotic areas varies widely with plant species, coinciding with the vein endings in the leaf where B accumulates to high concentrations (Case study 16.1).

Reproductive development is especially sensitive to B deficiency and there are many reports of depressed seed production in crops and pastures with no visible symptoms of B deficiency in vegetative tissues. In subterranean clover (New South Wales production) poor seed production in legumes and other dicotyledons results from inhibition of flowering, shedding of flowers and fruits and poor seed development. Seeds with low B concentrations may also fail to germinate or produce malformed seedlings. In cereals and other monocotyledons, B deficiency depresses seed production by lowering pollen viability and growth.

Many of the characteristic symptoms of B deficiency may be related to some requirement for B in cell wall for-mation. Most B in cells on a marginal B supply is tightly bonded to cell walls, and differences in cell wall composition explain a much higher internal B requirement by dicotyledons compared to monocotyledons.

B deficiency has affected crop production in many countries and especially across South Asia, although susceptibility to B deficiency varies widely among cereals and legumes. B deficiency has not been a widespread problem of crops and pastures in Australasia, but B toxicity occurs in cereals in South and Western Australia on soils formed from parent material of marine origin. Genetic variation in cereals with respect to B absorption has allowed breeding and selection for cultivars tolerant to high B soils (Case study 16.1).

(c)  Deficiencies of group 3 nutrients: K, Ca, Mg, Na, Cl


Plant K is present in solution and adsorbed into cellular com-ponents as a univalent cation. K activates more than 50 enzymes and has major roles in membrane transport in osmotic and pH balance of cell cytoplasm and vacuole. K is transported into and out of guard cells as a counter-ion for malate, in the process controlling the opening and closing of stomata (Section 15.2). K is highly mobile within plants, and following onset of deficiency K moves rapidly from older leaves to young organs. Symptoms of K deficiency generally appear first on recently matured leaves and include a general bronzing discolouration or an interveinal chlorosis followed by necrosis described as ‘scorching’. Symptoms of K deficiency on legumes are often sufficiently specific for reliable diagnosis, namely a characteristic pattern of white spots that develops on mature leaves and becomes necrotic, resembling insect damage.

Plants require K in large amounts, second only to N. In some species such as sugar beet and others with halophytic relatives, Na can substitute for K in large part, probably by meeting osmotic functions normally attributed to K. Other species exist where Na/K substitution never occurs, and between these two extremes species and even cultivars vary widely in their Na/K flexibility.

With the exception of areas of light sands, which are especially widespread in Western Australia, most Australian soils contain adequate K for plant growth (clay soils derived from illite are especially well provided with reserves). In the sandy soils mentioned above, K is adsorbed onto organic matter as an easily exchangeable univalent cation which is readily leached. On such soils, development of a soil horizon to trap leached K within reach of plant roots assumes especial importance. Large amounts of K are also leached from living leaves and contribute to K mobility within ecosystems.

K content of actively metabolising cells is high (2–5% dry mass) but declines rapidly with senescence. As a result, removal of green plant material as hay also removes large amounts of K which in turn can induce K deficiency on soils with low reserves.

Sodium and chlorine

Deficiencies of these nutrients have only been seen in plants grown in highly purified environments; they have not been observed in natural or agricultural ecosystems. By contrast, toxicities of Na and Cl are widespread and cause serious problems in many countries (Section 17.1)

Na may benefit plants in any of three distinct ways: Na may be essential; Na may substitute for K when K supply is low; and Na may enhance growth even when K supply is high. Brownell and his colleagues at the universities of Adelaide and then at James Cook in Townsville have established the essentiality of trace amounts of Na for C4 plants (Feature essay 16.2).

Calcium and magnesium

Deficiencies of Mg are rare in Australia but have been reported for fruit and vegetable crops in New South Wales and Western Australia; citrus trees are especially sensitive. In some cases the deficiency has been induced by heavy appli-cations of K or ammonium fertilisers to acid soils. Mobility of Mg from leaves is intermediate between that of the highly mobile K and immobile Ca and is greatly accelerated by senescence. Mg deficiency symptoms generally appear first in older leaves as interveinal chlorosis but may appear first in young leaves depending upon the rate of development of the deficiency and other environmental factors. Chlorosis results from the breakdown of chlorophyll which has Mg covalently bound in its centre. Each molecule of chlorophyll carries one Mg atom, but in terms of the total pool of leaf Mg, the amount bound to chlorophyll varies from around 35% of total leaf Mg in deficient leaves to 5% in leaves with more than adequate Mg. Another 5–10% of leaf Mg is bound in the cell walls. Remaining Mg is largely ionic and functions as an osmoticum and as a catalyst in a wide range of reactions including phosphorylations and carboxylations.

Ca deficiencies are more common than Mg deficiencies, but are usually restricted to small areas of acid soils or occur sporadically as physiological disorders in particular crops. On acid peaty sands in Western Australia symptoms of Ca de-ficiency have been observed in clover, and were accompanied by symptoms of N deficiency due to low Ca inhibition of N2 fixation. Application of calcium carbonate corrected both deficiences. Calcium carbonate, despite being only sparingly soluble, was more effective than calcium sulphate because it decreases acidity which inhibits Ca absorption. Although Ca deficiency is relatively rare, calcium carbonate has been widely used to correct a variety of other problems associated with soil acidity (Section 16.5).

A number of puzzling physiological disorders have been recognised as being due to Ca deficiency and attributed to the low mobility of Ca in phloem. These include bitter pit in apples, brown heart in compact leafy vegetables such as brussel sprouts and lettuce, empty pods in peanuts and subterranean clover, and blossom-end rot of tomatoes. Because of the low mobility of Ca in phloem, developing organs must obtain their Ca requirements from the xylem sap or directly from external sources. Fruits and leaves receive their Ca supply in the xylem sap and hence are affected by factors limiting their rates of transpiration, especially humidity. Roots and under-ground fruits, such as peanut and subterranean clover pods, receive little or no inflow of xylem sap, so must obtain their Ca from the surrounding soil.

The low phloem mobility of Ca also results in symptoms of Ca deficiency appearing in growing apices and young regions of the shoot and stem. Following exhaustion of Ca supply, symptoms also appear in older organs as a result of later cell expansion or loss of Ca via exchange with other cations in the xylem sap.

(d)  Deficiencies of group 4 nutrients: Mn, Fe, Co, Ni, Cu, Zn, Mo


The first symptoms of Mn deficiency in plants frequently resemble those of Fe deficiency (Figure 16.8) with interveinal chlorosis developing in the youngest leaves and often requiring biochemical tests or elemental analysis for definitive diagnosis. Sometimes interveinal chlorosis develops first in mature leaves apparently at variance with low mobility of Mn from these leaves. While interveinal chlorosis is the first visible symptom, photosynthesis may be severely depressed before chlorophyll concentration is affected. Water photolysis (Section 1.1) is catalysed by an Mn metalloenzyme in which Mn undergoes reversible oxidation–reduction. Only one other Mn metalloenzyme is known — MnSOD. But, unlike other nutrients in this group, much of the Mn is present as divalent ions which act as cofactors to over 30 other enzymes catalysing key metabolic events including oxidation–reduction, de-carboxy-lation and hydrolytic reactions.


Figure 16.8 Visible leaf symptoms on sweet potato, representative of deficiencies in N, P, K, Fe, Mn, Cu and Zn. N deficiency (a) in cultivar Wanmum results in small pale leaves with a dull appearance (left side) compared with larger, deeper green and more lustrous full-nutrient control leaves (right side). P deficiency (b) on young leaves of cultivar Markham produces a characteristic red-purple pigmentation on upper surfaces. K deficiency (c) leads to interveinal chlorosis in mature leaves which becomes accentuated around leaf margins and finally necrotic lesions on oldest leaves. Fe deficiency (d) in cultivar Markham results in sever bleaching of young leaves while old leaves with adequate Fe remain deep green. Mn deficiency (e) results in chlorosis, leaf drooping, puckering and downward rolling of leaf margins, and eventually a development of interveinal pitting. Cu deficiency (f) in cultivar Wanmum produces a diffuse interveinal chlorosis and drooped appearance in deformed leaves which eventually form necrotic lesions. Holes sometimes form in older leaf blades due to uneven expansion. Zn deficiency (g) in four cultivars where young leaves from low-Zn plants (right side of picture) are compared with full-nutrient leaves of equicalent age on healthy plants. Cultivars top to bottom are Lole, Hawaii, Markham and Wannum. (Based on O'Sullivan et al. 1997)

Mn deficiency also depresses lignin synthesis, especially in roots. Low lignin content of roots is thought to be responsible for the low resistance of Mn-deficient plants to root diseases such as ‘take all’ (Graham and Rovira 1984).

In peas and lupins with little or no vegetative symptoms, Mn deficiency sometimes affects seed production inducing symptoms such as marsh spot in peas and split seed in lupins which are sufficiently specific to diagnose Mn deficiency unambigously.


Table 16.5

Mn deficiency is an important problem for crops in many countries, and occurs on acidic soils containing low concen-trations of Mn and on calcareous soils. Plant-available Mn in soils fluctuates widely and rapidly with environmental con-ditions, increasing with acidity, soil water and anaerobiosis, and decreasing with alkalinity, decreasing soil water and aerobiosis. On calcareous soils, such as those of the Cape Yorke Peninsula in South Australia, Mn deficiency is particularly difficult to correct as any Mn fertiliser is rapidly immobilised in the soil. This situation provides a compelling argument for continuing research into genetic factors underlying mechanisms of Mn uptake from soils and especially species differences in acquisition (Table 16.5).


The first symptoms of Fe deficiency generally appear as chlorosis in the youngest leaves, reflecting both the retention of Fe in older parts and a function of Fe in chlorophyll synthesis (Figure 16.8). In legumes, older leaves may also become pale due to Fe deficiency inhibiting nodule development.

Fe is also involved in many other plant processes as it is an essential component of many enzymes in which it acts either as a bridging agent to substrates, as in the S–Fe protein aconitase, or as a redox agent, as in heme enzymes such as cytochrome and in S–Fe proteins such as ferredoxin and superoxide dismutase.

Fe deficiency is a serious and widespread problem of crops in many countries but is relatively unimportant in Australia. Fe deficiency is common on calcareous soils where its severity has been correlated in non-gramineous plants with the amounts of poorly crystalline and amorphous Fe oxides and in gramineous plants with HCO3 concentrations. These different relationships arise from differences between the two plant groups in the response of their roots to Fe deficiency.
In gramineous plants, the onset of Fe deficiency promotes excretion of organic compounds with the capacity to chelate Fe (phytosiderophores) in soluble complexes which may then be absorbed and metabolised. By contrast, Fe deficiency in non-gramineous plants promotes the excretion of hydrogen ions, solubilising soil Fe by acidification of the rhizosphere; high concentrations of HCO3 counteract this mechanism by buffering the rhizosphere against acidification.


Co is required by legumes for N2 fixation but not for growth of plants given adequate fixed N. Within legume nodules, Co is chelated to N atoms in the centre of the porphyrin structure of cobalamin, which is an essential coenzyme for several enzymes involved in the metabolism of bacteroids and free-living Rhizobium and other N2-fixing organisms. In legumes the symptoms of Co deficiency are those of N deficiency from delayed nodulation or impaired fixation once nodulated.

Co deficiency in plants is rare in the field but has been demonstrated in subterranean clover on impoverished siliceous sands in South Australia and Western Australia and in lupins on lateritic sandy soils in Western Australia. The amount of Co required is very small and seeds may contain sufficient for the current crop; indeed, the first appreciable field response of lupins to Co was obtained in a crop sown with seed saved from two previous generations on the same soil!

By contrast, Co deficiency in sheep and cattle has been a serious and widespread problem over appreciable areas of New Zealand, southeastern South Australia, and southern Western Australia. Milder deficiencies occur in many other countries.


During the 1990s and some years after plant urease was shown to be an Ni metalloprotein, Ni was shown to be essential for legumes and cereals. One of its functions probably involves detoxification of urea. So far, no unequivocal demonstration of Ni deficiency has been shown in field crops although Ni toxicity occurs on both natural and polluted soils.


Cu deficiency has been a widespread and serious problem in crops, pastures and animals in many countries, including Australia. In plants, Cu is an essential component of many enzymes and non-enzyme proteins involved in electron transfer in many processes including photosynthesis, respiration and lignification. Cu is also required for N2 fixation in legumes, but the amounts required are very close to those for growth so that, while symptoms of Cu deficiency may appear as N deficiency, they often develop other characteristics as the deficiency becomes more severe. Except where N2 fixation is involved, symptoms appear first in young leaves and meristems owing to the low mobility of Cu from older leaves before they senesce.

Symptoms often appear as a distortion of young leaves and stems, death of apical meristems with multiple bud develop-ment, leaves with interveinal chlorosis (Figure 16.8) or which are blue-green in colour, and appearance of wilting with flaccid leaves and pendulous branches. Wilting and twisting and distortion of leaves, as characterises Cu deficiency in many species, may be ascribed to poor lignification related to the low activities of two Cu enzymes involved in the synthesis of lignin — polyphenol oxidase and diamine oxidase. Lignin synthesis is sensitive to mild Cu deficiency so that a simple lignin staining test on cut stems may be used to diagnose Cu deficiency in plants.

As with Mn deficiency, poor lignification of roots may account for the susceptibility of Cu-deficient plants to root diseases such as ‘take all’. Poor lignification of anthers in Cu-deficient plants also leads to their failure to open and release their pollen. In addition, pollen from Cu-deficient plants may be sterile. As a result, seed production is particularly suscep-tible to Cu deficiency and wheat crops with no leaf deficiency symptoms have been found at harvest to have set few seed.


The most characteristic symptom of Zn deficiency in dicotyledonous plants is the appearance of a rosette of little, misshapen leaves at the stem apex leading to descriptions of the disorder as ‘rosetting’ and ‘little leaf’. Zn deficiency is usually accompanied or preceded by an interveinal chlorosis and necrosis of older leaves and sometimes also by their discolouration from accumulation of anthocyanins. In cereals and other monocotyledons only the symptoms on the older leaves are obvious.

Misshapen leaves and a failure of stem internodes to elongate in rosetting led to the hypothesis over 50 years ago that Zn was required for synthesis of indole acetic acid (IAA). IAA concentrations are depressed in apices of Zn-deficient plants and recover quickly on addition of Zn, but a specific role for Zn in its synthesis has yet to be defined. Meanwhile, Zn has been shown to be a component of many metalloenzymes, to be essential for ribosome structure and integrity of membranes, and as Zn2+ to activate enzyme systems. Of the many Zn metalloenzymes, one is involved in gene expression through its binding to DNA, affecting its replication and transcription. This function, together with roles in preserving the structural integrity of ribosomes and in depressing RNase activity, gives Zn a key role in protein metabolism and creates a high requirement for Zn at sites of protein synthesis. As a result, meristematic tissues accumulate high concentrations of Zn; young leaves also have much higher internal Zn requirements than older leaves so that critical Zn concentrations for diagnosis of Zn deficiency vary widely with leaf age.

Zn deficiency has been a widespread problem in many countries, occurring in both acid soils with parent materials containing low Zn and calcareous soils where low pH makes Zn unavailable. Zn has been a particularly important deficiency in southern and western Australia, severely depressing both legume and cereal production. The deficiency would have been even more severe and widespread had Zn not been a contaminant of many macronutrient fertilisers including superphosphate. With replacement of superphosphate by P fertilisers with lower Zn contents, crops in soils considered from previous experience to have adequate Zn now show Zn deficiency.


Symptoms of Mo deficiency and plant requirements vary with species and environmental conditions. In legumes and other N2-fixing plants on soils low in N, Mo deficiency is expressed as an N deficiency due to failure of N2 fixation by a symbiotic system that requires Mo for nitrogenase. In all plants supplied with adequate N as nitrate, leaves may become pale, malformed and necrotic as N metabolism fails and nitrate accumulates to toxic levels due to low activity of the Mo metalloenzyme nitrate reductase. Plants with adequate nitrate supply need much less Mo than plants fixing N2. Plants supplied with N as ammonium under sterile conditions require only very small amounts to forestall symptoms.

Variation in expression of Mo deficiency in crops and pastures reflects differences in Mo requirements for particular functions such as symbiotic N2 fixation. Mo deficiency was thus a widespread problem in pastures where legumes were sown to improve N status of low N soils (Figure 2 in Feature essay 16.1). Mo is particularly important for legume-based pastures on acidic soils in eastern Australia. Responses of non-leguminous crops to Mo are much more restricted.