Manganese deficiency

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Characteristics and occurrence

Manganese (Mn) is present in the soil as free Mn2+, which is readily available to plants, and as oxides of low solubility. The proportion of manganese in various forms in the soil is dependent both on chemical reactions and on microbial activity. High soil pH greatly reduces the solubility of soil manganese, and therefore its availability to roots. Thus, manganese deficiency is most likely to occur in soils that are alkaline or have been limed.

There have been few confirmed field observations of manganese deficiency in sweetpotato reported in the scientific literature. It has been reported in sweetpotato grown on coralline soils near Madang, Papua New Guinea, although sweetpotato was much less affected by the disorder than was yam (Dioscorea esculenta).

Microbial activity in the soil results in the oxidation of Mn2+ to insoluble higher oxides. As this is favoured in well-aerated soils, manganese deficiency may arise intermittently during drier periods, or appear more severe in well drained parts of the field. Cycles of manganese deficiency and recovery may result in symptoms normally associated with young leaves appearing on older parts of the plant.

Symptoms

Usually the first sign of manganese deficiency in sweetpotato is an indistinct interveinal chlorosis throughout the plant, but particularly on leaves of intermediate age. The green zones around major veins are relatively broad and fade gradually toward the interveinal zone. In some cultivars, the chlorosis may appear more general than interveinal. Chlorosis may be accompanied by drooping of the leaves, slight puckering of the leaf surface or downward curling of the leaf margins. The drooping is caused by bending of the petiole and is not accompanied by wiltingof the leaf blades, nor does it progress to the point of leaf senescence and abscission.

On young, expanding leaves, small areas between minor veins become pale and sunken, and eventually develop into necrotic spots. While all interveinal zones of the leaf are affected, they do not develop at the same rate. Indeed, it is common to see a peppering of brighter, cleared spots across the leaf blade and  necrotic pits develop.  Initially, the leaves most affected are those which are rapidly expanding, a few nodes back from the tip. But as the symptom intensifies, both older and younger leaves are affected. Pits in older leaves tend to be darker and are often concentrated near the base of the midrib and main veins. The young leaves become pale, thickened and brittle, and may curl under or buckle as they expand. When pitting occurs in very young leaves, their subsequent expansion causes the pits to develop into larger holes. In severe cases only a lacy skeleton of the leaf remains. Severely-affected leaves become necrotic, the necrosis spreading from the tip or lateral margins. The growing points at the shoot tip and in leaf axils remain active. Axillary shoots are generally less affected than the subtending leaf.

In cultivars where the leaf blade is deeply divided into lobes, the above symptoms may be poorly developed. Instead, small, chlorotic, thickened and deformed young leaves may be produced. The leaf surface may be finely pitted especially in the vicinity of main veins.

Pillai et al. (1986) reported that manganese-deficient plants produced small, thin storage roots which had brownish streaks in the flesh.

Possible confusion with other symptoms

Copper deficiency may also induce interveinal chlorosis and drooping in mature leaves, but in the case of copper deficiency, there is a distinct wilting of the leaves, and this may progress to leaf senescence and abscission. This does not occur with manganese deficiency. The appearance of small, deformed young leaves may also be mistaken for copper deficiency, although the latter does not typically induce chlorosis or pitting of the leaf surface.

The clearing of small islands of interveinal tissue may also be a symptom of copper toxicity. In this case, however, the chlorosis usually only affects mature leaves, and may occur on only localised areas of the blade. Symptoms of manganese deficiency tend to be expressed in young leaves, uniformly across the leaf blade.

Diagnostic soil and plant tissue tests

A critical concentration of 19 mg Mn/kg in the 7th to 9th youngest leaf blades was determined in solution culture studies using cv. Wanmun. In healthy plants, concentrations were generally between 26 and 500 mg Mn/kg.

Manganese availability in the soil may be estimated by extraction with a chelating agent such as diethylenetriaminepentaacetic acid (DTPA). Concentrations of DTPA-extractable Mn less than 4 mg/kg are considered potentially deficient for a range of root and vegetable crops.

Suspected cases of manganese deficiency can be confirmed by leaf painting with a 1% solution of manganese sulfate. Manganese application causes regreening of chlorotic tissue, and in young leaves it arrests the development of interveinal pits and enhances expansion of the treated portion of the leaf blade.

Management

Cultural control

Except on some sandy soils, manganese deficiency usually arises due to soil conditions which limit the availability of manganese to plants. Therefore, fertilisation of the soil with manganese may be ineffective, as the added manganese may become unavailable. Foliar sprays of 0.1% manganese sulfate or chelate, at 2 to 4 kg Mn/ha, may be effective. The elevation of soil organic matter content, by mulching or composting, will help to improve the availability of manganese and other nutrients to the crop.

When deficiency occurs at neutral to acidic soil pH, manganese may be applied to the soil, as either manganese sulfate or oxide. Rates used for other crops are typically in the range of 10 to 20 kg Mn/ha. Soils low in manganese should not be limed above pH 6.4 (measured in water).

References

CFL 1983. Soil Analysis Service Interpretation Charts. Consolidated Fertilizers Limited, Morningside, Queensland, Australia.

Johnston, M. 1996. Nutrient disorders of root crops growing on raised coral reef landforms near Madang, Papua New Guinea. In: Craswell, E.T. Asher, C.J. and O’Sullivan, J.N. (eds.) ACIAR Proceedings No.65: Mineral nutrient disorders of root crops in the Pacific. pp 127-129.

O’Sullivan, J.N., Asher, C.J. and Blamey, F.P.C. 1997. Nutrient Disorders of Sweet Potato. ACIAR Monograph No. 48, Australian Centre for International Agricultural Research, Canberra, 136 p.

Pillai, N.G., Mohankumar, B., Kabeerathumma, S. and Nair, P.G. 1986. Deficiency symptoms of micronutrients in sweet potato (Ipomoea batatas L.). Journal of Root Crops 12 (2), 91-95.

Rayment, G.E. and Higginson, F.R. 1992. Australian laboratory handbook of soil and water chemical methods. Inkata Press, Australia.

Contributed by: Jane O'Sullivan

Characteristics and occurrence

Symptoms

Confusion with other symptoms

Diagnostic tests

Management

References


Mottled interveinal chlorosis with drooping and curling of margins (J. O'Sullivan).

Bright translucent spots on young expanding leaves are often the earliest conspicuous sign (J. O'Sullivan).

Close-up, tiny pockets between minor veins are seen to become pale, then sunken and necrotic (J. O'Sullivan).

Pits developing on a more mature leaf tend to be less translucent and more sunken, while those formed on very young leaves form holes as the leaf expands (J. O'Sullivan).

 Even in severe cases, the shoot tip usually stays alive, but leaves develop symptoms as they expand (J. O'Sullivan).