In this article we will discuss about the corn smut caused by basidiomycetes.
Host: Zea Mays
Pathogen: Ustilago maydis
Introduction to the Corn Smut:
Corn smut disease is worldwide in its distribution. In India the disease occurs wherever com is grown particularly in the Punjab, U.P. and Kashmir. It is known as Kangiari.
Importance of Corn Smut Disease:
The amount of damage resulting from this disease in India is not much. Much importance is, therefore, not given to the disease in this country as compared with other countries, particularly America.
The damage includes sterility of the diseased plants. There is reduction in yield and amount of fodder, inferior kernel lustre of smutted ear and lower carbohydrate content.
Symptoms of Corn Smut Disease:
The disease is easily recognisable by the presence of large knob-like sooty swellings or boils known as the smut galls or balls tumours (Fig. 22.16 E). No other symptoms appear on the host plant before the formation of smut ball. The latter appear on ears or stems (stalks).
Tumours are also formed on the leaves and tassels (male flowers). They are, however, much smaller in size. The galls at an early stage are light coloured and are edible. At this stage they are covered with a firm shining membrane.
It is greenish white in colour. Towards maturity the tumours turn sooty due to spore formation inside. The covering membrane gradually dries and finally bursts to expose the sooty, powdery mass of smut spores.
The disease is localised and not systemic. Each tumour is the result of a separate and distinct infection. Unlike other cereal smuts the fungus mycelium does not pervade the entire plant. Infection takes place through the meristematic (embryonic) tissue of the over ground parts of the host plant such as stems, leaves, ears and tassels.
Com smut thus provides an example of general infection through any embryonic tissue. Infection takes place any time during the growing season. In case the infection takes place through the silk, tumours are formed in place of kernels.
Causal Organism:
The disease causing organism is U. maydis (Dc) Cda. The black, generally spherical to ellipsoidal, heavily echinulate smut spores are the resting spores. They over-winter on the crop refuse in the soil or in the manure of cattle fed on the diseased corn.
Disease Cycle (Fig. 22.16):
The primary inoculum comes from the air borne and water borne sporidia or basidiospores which are produced by the teliospores overwintering on crop refuse or in the soil rarely on the grain itself (A). The teliospores are spherical to ellipsoidal in form, black in colour and echinulate. Each measures 8 to 11 µ in diameter.
(a) Germination of teliospores (B1-3):
They germinate under suitable conditions of temperature and moisture. Each grows into a septate, slender promycelium called the epibasidium. It is a four-celled structure (B2). Each segment of the epibasidium bears an ovate, unicellular, hyaline basidiospore or sporidium (B3). The sporidia multiply by budding in a yeast-like manner.
(b) Germination of basidiospores and infection:
The sporidia are dispersed by air currents (C) or water. They fall on the corn plant. According to Walter (1934), the embryonic tissues of all above ground parts are susceptible to direct penetration. Here each basidiospore germinates by producing a germ tube or a primary hypha (D).
It directly penetrates the com tissue. Entering the epidermis it grows horizontally beneath it to form a primary or monokaryotic mycelium. Active infection takes place only when the two hyphae from neighbouring primary mycelia of opposite strains come in contact.
The intervening walls between the vegetative cells of the hyphae dissolve at the point of contact. It is an example of somatogamy. The fusion cell thus formed contains a pair of nuclei of opposite strains. They lie side by side to form a dikaryon.
The fusion cell containing the dikaryon is called the dikaryotic cell. By elongation and clamp connections, it develops into a dikaryotic or secondary mycelium. The latter carries on the role of parasitism. It grows vigorously and is largely intercellular.
(c) Formation of Galls or Tumours:
In response to fungus infection the host cells in the infected region increase in size (hypertrophy) and in number (hyperplasia). Consequently a tumorous outgrowth develops. It is permeated with the secondary mycelium.
The fungal hyphae at this stage become additionally septate into smaller binucleate segments. These segments round off and separate into binucleate smut spores. Meanwhile the host tissue in the tumour, excepting the superficial layer, disintegrates.
The tumour is now filled with a mass of myriads of black smut spores (E). The covering membrane dries and finally ruptures to release the smut spores. They are blown about by the wind and dispersed. Eventually they return to the soil and remain dormant in winter.
Control Measures of Corn Smut Disease:
Rotation of crops and sanitation are helpful but do not offer complete control. They simply assist in reducing the damage. Collecting the smut tumours from the field before smut spores are released and burning them is a useful control measure.
The best control measure is to grow the most resistant com hybrid available. The infection incidence can also be reduced by the application of insecticides such as DDT, Nicotine etc.