Bladder smut attacks corn in most growing areas. It is distinguished from loose smut by the fact that it appears in the form of galls (the so-called pathological formations) on all organs of corn. Often such galls can be observed on cobs with leaves. Corn is considered to be most susceptible to this ill-fated scourge at the stage from the moment the panicles are thrown out and up to the stage of milky ripeness, so during this period special care should be taken, otherwise yield losses can reach 25 - 30%, and in dry conditions - even 50%.
A few words about the disease
When corn leaves are affected, one can observe the appearance of swellings that resemble groups of rough wrinkles in appearance. And in the panicles, isolated flowers are mainly affected, on which the formation of small bag-like swellings begins. In this case, quite large galls are formed on the ears with stalks, in which fungal teliospores develop. The spores ripening in such galls slowly germinate and attack the corn throughout the growing season. The finally mature swellings consist of black spore masses covered with grayish and shiny fleshy membranes.
With the onset of autumn, smut swellings often break off during corn harvesting and often overwinter in corn fields. And in the spring, the activated spores again infect the plants.
The causative agent of bladder smut is a basidiomycete fungus called Ustilago zeae Unger. When its mycelium matures, many harmful spores are formed. In the mass they are usually colored in black-olive tones, and the spores located individually are spherical in shape and colored yellow-brown. They are often equipped with large bristles and decorated with a mesh pattern.
To a large extent, the development of this ill-fated scourge is facilitated by dense crops, light rainfall during the infection period and dry weather. This disease is especially harmful when it affects corn stalks and cobs. Its development is also affected by soil moisture. Plants are much less affected in cases of moderate humidity. But with high or low soil moisture, their susceptibility will be much higher. Sudden fluctuations in humidity also increase susceptibility - this feature is important to take into account if corn is cultivated on irrigated lands.
Corn attacked by blister smut is much more susceptible to stem rot. And if this dangerous disease affects young plants, they can easily die. And in general, the harmfulness of this scourge is very great, because it provokes infertility of the cobs and a significant crop shortage (sometimes up to 60%).
Corn smut can often be encountered in areas with insufficient or unstable moisture, as well as in the south of the European part of the former USSR.
As for the toxicity of the growths formed as a result of infection with bubbly smut, biologists have differing opinions. Most of them believe that young growths in the absence of teliospores cannot be poisonous, but old growths filled with a huge number of teliospores are comparable in toxicity to ergot.
How to fight
The main protective measures against harmful bubbly smut are the selection of healthy and strong seed cobs and timely removal of post-harvest residues from areas.The problem of seed infection can be solved by treating the seeds. The Lanta disinfectant copes well with this task. And seeds should be sown only in well-warmed soil. However, it is important not to forget that infection can occur later. A fairly effective means of control will be the selection of resistant hybrids, as well as their proper spatial isolation.
Belongs to the higher fungi of the class Basidiomycetes, subclass Teliomycetes, order Golovnevye.
Cultures.
Affects corn.
Prevalence.
It is found in all regions of the Russian Federation where corn is cultivated.
Symptoms of the disease.
The disease affects corn throughout the growing season. It is characterized by the formation of whitish swellings and nodules of various sizes. On shoots and nodes it appears in the form of spherical-tuberous swellings with a diameter of up to 15 cm or more. On the leaves, swellings form along the veins and have an elongated shape. On the cobs, individual ovaries are affected, the development of which is delayed or stopped. They may also grow and take on an irregular shape. On sultanas, individual flowers are affected, which grow, forming blisters.
Biology of the pathogen.
At sites of infection, a pale or greenish-yellow swelling forms on all plant organs. Later, by the time the teliospores mature, the nodule darkens and is covered on top with a whitish-gray film that takes on a silvery sheen. Later, the nodule dries out, the covering film cracks and the released teliospores disperse, causing secondary infection. Some teliospores are retained in the affected ears of grain and in the field on post-harvest residues. Teliospores are able to germinate immediately as soon as they ripen, but in dry form they can persist for 5 years or longer. In natural humid conditions, they quickly lose germination, but, remaining in undisintegrated lumps in the field, they can serve as a source of primary infection for seedlings. Teliospores can also be introduced into the field with seed material. Teliospores, germinating, form basidia with basidiospores, which reproduce by budding. Sporidia sprout with growth tubes and penetrate only into young meristematic tissues. Haploid hyphae are formed from the germ tubes. The yield of green mass of corn due to disease is reduced by 25...50%, grain - by 50%.
Sources of infection.
Infected ears, plant residues, soil.
Preparations for protection.
Agrotechnical control measures.
Introduction to the production of resistant varieties, scientifically based seed production, compliance with crop rotation. Compliance with spatial isolation of seed plots from commercial crops, disinfection of agricultural machinery and equipment.
Distributed in all corn growing areas. It appears on cobs, plumes, stems, reproductive buds, leaves and aerial roots in the form of bubble-like swellings (galls) of various shapes and sizes. The disease is not detected on the roots. The development of the swelling begins with a pale, slightly swollen spot, which gradually grows and turns into a large nodule, filled first with white pulp, and later with a grayish-white or pinkish mucous mass, which then turns into a black-olive dusty mass of spores. The largest swellings occur on the cobs and stems. On the leaves they are usually small in the form of a group of rough wrinkles, often drying out to form spores.
Symptoms of the disease are first detected on young leaves and their sheaths, and sometimes on aerial roots located on the stem.
Severe damage is observed on seedlings when the apical bud is infected. Infected tissues of the buds (leaf and stem primordia) turn into smut growths and grow greatly, many times exceeding their original volume, as a result of which the impression of “diffuse” damage to the plant is created.
From the phase of 5-8 leaves, damage to leaves, leaf sheaths and stems is detected. Then the disease appears on the panicles, and from the beginning of flowering and with the appearance of stigmas, the ears are affected. After emergence and the beginning of flowering, axillary buds located under the leaf sheaths and below the cobs become infected.
The most severe form of the disease is damage to the stem. In this case, the plant becomes distorted, the entire part of it above the affected area turns into smut growths and dies.
The causative agent of the disease is the basidiomycete fungus Ustilago zeae Unger of the order Ustilaginales. When the swellings ripen, its mycelium breaks up into a huge number of teliospores. In mass they are black-olive, and single ones under a microscope are yellow-brown, spherical, with a mesh pattern and large bristles, 8-13 microns in diameter.
When the swelling shell bursts, teliospores scatter across the field and serve as a source of infection of young plant organs. They germinate in the presence of dripping moisture within a few hours. The optimal temperature for their germination is +23-25°, at + 15...18° it slows down, and at 12° and below it stops. In germinating teliospores, after 15-20 hours, a rapidly developing sprout appears - the basidium, on which unicellular colorless elongated basidiospores measuring 3 X 1.2 microns are formed. They often reproduce by budding, producing large numbers of sporidia, which are sometimes called secondary conidia.
The hyphae of the haploid mycelium coopulate with the hyphae of the mycelium of the opposite sex and give rise to the development of a diploid mycelium, consisting of thick knotty hyphae. From the diploid mycelium, after 20-24 days, a swelling with teliospores develops at the sites of infection.
During the growing season of corn, the fungus can produce 3-4, and sometimes 5 generations, which explains the strong manifestation of the disease at the beginning of harvesting.
The fungus U. zeae does not spread diffusely throughout the plant, so each swelling forms in the area where the plant was infected.
Dry teliospores can remain viable for up to four years, whereas in natural conditions, when exposed to water wetting, they quickly lose their viability. However, teliospores, which are in the form of lumpy swellings, are poorly wetted and do not die during autumn, winter and spring. In the spring, when cultivating the soil, they break up and the spores are carried by the wind, being the primary source of plant infection. In rare cases, the pathogen may be introduced into the field with seeds, which sometimes retain viable teliospores.
The degree of development of bladder smut depends on soil moisture. At optimal humidity (60% PV), plant damage is always less than at low (40%) or high (80%). Fluctuations in soil moisture lead to increased damage to plants, which should be taken into account when cultivating corn on irrigated lands (Shkodenko V.I., 1966).
The harmfulness of blister smut lies in the death of affected young plants, infertility of cobs when infected early and a significant loss of yield. The latter depends on the size and number of swellings on the plant. With large swellings, the yield is reduced on average by 60%, with medium swellings - by 25, small ones - by 10%. The harmfulness of two swellings on one plant is three times greater than the harmfulness of one same swelling (Nemlienko F. E., 1957).
When studying the characteristics of the development of bladder smut against the background of natural and artificial infection, T. A. Kulik (1975) found that the formation of galls is determined by genotypic differences in self-pollinated lines and the reaction of the host plant to the introduction of the pathogen.
Data on the toxicity of bladder smut are contradictory. Most authors believe that young growths in which teliospores have not yet formed are non-toxic, and when the latter form, they can be as toxic as ergot. Therefore, parts of plants affected by bladder smut are not recommended for use as animal feed.
The main measures aimed at protecting corn from smut are observing scientifically based crop rotation, breeding and zoning of resistant hybrids and varieties, seed treatment, sowing at optimal times and at optimal depth, applying phosphorus-potassium fertilizers, removing post-harvest residues, spatial isolation seed plots at least 1 km from fields where corn was grown in the previous year.
The pathogen infects young plant tissues at all stages of plant development throughout the growing season. Initially, the sites of infection lighten and transform into a mucous mass of bluish-white color. Towards the end of development, the overgrown nodules turn into an olive-black mass of dusty spores. A characteristic sign of the disease is the formation of bubble-like nodules of various shapes and sizes on the above-ground parts of plants. The diameter of one formation can exceed 15 cm. In case of infection, the growth points of the nodules spread linearly, giving the impression of a systemic development of the disease. The most dangerous is the appearance of formations on the stem. In this case, deformation and often drying out of the entire plant occurs. On leaf blades, nodules form after the formation of 5–8 leaves. Here they are small, collected in groups. The reproductive organs are affected by blister smut simultaneously with the ejection of the panicle and the beginning of flowering. With a strong degree of development of the disease, their death may be observed. (Stancheva Y., 2003)
Young ovaries die when infected. When the stalks of anthers and bracts are damaged, nodules are formed in panicles. In this case, the anther shells may become infected. This leads to the death of pollen grains. (Peresypkin V.F., 1989) The cause of the disease is a basidiomycete from the order Ustilaginales –Ustilago zeae.
Teliospores in the mass black-olive in color, individually yellow-brown, spherical in shape with a mesh pattern and large bristles on the surface. (Peresypkin V.F., 1989)
Basidiospores colorless, unicellular, oblong. (Peresypkin V.F., 1989) The pathogen has a large number of physiological races. (Stancheva Y., 2003)
Biology
Primary infection of plants occurs in the spring. Usually, during plowing of the soil, mechanical damage to overwintered mature nodules occurs. In this case, teliospores scatter and infect plants. The spores infect only growing plant organs. Under favorable conditions, in the presence of dripping moisture and temperatures above + 12 °C, teliospores germinate. The optimal temperature for spore development is +23 °C + 25 °C. In germinated spores, within 24 hours (after 15-20 hours), a basidium with basidiospores is formed, which reproduce by budding and form many secondary conidia (sporidia). Sporidia and basidiospores tolerate lack of moisture for up to 35 days. With sufficient moisture, basidiospores and sporidia, and sometimes the basidia themselves, form a germ tube that can penetrate the plant only through the epidermis of young tissues. Within the plant tissue, the germ tube forms a haploid filamentous mycelium, the hyphae of which copulate and form a diploid mycelium with thick, knotty hyphae. After 20–24 days, swellings with maturing teliospores form from the mycelium. After ripening, the swelling disintegrates and the spores scatter. During the growing season, the pathogen is capable of producing up to five generations, which contributes to the development of a strong degree of infection of crops. The pathogen is not able to spread by diffusion throughout plant organs. Each swelling is an independent infection. The disease affects only vegetative cells. For example, in grains the outer shell of the pericarp is infected, while the endosperm, embryo and nucellus are not affected by the pathogen. In conditions of low humidity, chlamydospores of bladder smut remain viable for up to four years. In field conditions, with periodic wetting with water, teliospores can quickly lose germination. Provided there is insufficient wetting of the lumpy swellings for the germination of teliospores in the autumn season, the nodules remain in the soil and overwinter successfully. Spring plowing of the soil leads to damage to the nodules and the spread of the pathogen. Sometimes the source of infection can be infected seeds. Soil moisture plays a significant role in the development of the disease. With optimal humidity, the infection develops minimally. An increase or decrease in humidity leads to an increase in the degree of damage to corn. (Peresypkin V.F., 1989)
Geographical distribution
Blister smut distributed everywhere in corn growing areas. (Shkalikov V.A., 2003)
Maliciousness
Blister smut It is considered one of the most harmful diseases of corn. The infection leads to the loss of young plants, the formation of infertile ears, as well as a significant drop in yield due to damage to various terrestrial organs: aerial roots, leaves, stems. Plants affected by the pathogen are not suitable for animal feed, either fresh or for ensiling, since the teliospores that form are toxic. (Peresypkin V.F., 1989)
Control measures
Agrotechnical
- plowing the soil in autumn;
- use of quality seeds;
- use of resistant varieties;
- compliance with sowing deadlines. (Stancheva Y., 2003)
Chemical
- dressing of seed material;
Fungicides: . (State catalogue, 2016)
V.G. Ivashchenko
Doctor of Biological Sciences, Professor
In the territory of the former USSR, the disease is widespread, more severe in the south of the European part in areas with unstable or insufficient moisture. In the 60s of the twentieth century, the infestation of plants in the steppe zone of Ukraine was 12-19% (Nemlienko, 1957), but in some years the infestation of corn in the Crimea reached 20-40% (Tikhonov, Tikhonov, 1960), in the south of Ukraine - 71 % (Klyuchko et al., 1976), in Moldova - 25-40% (Yurcu et al., 1982), in Primorsky Krai - 60-75% (Azbukina, 1962). With the increase in the area of corn for grain, silage and green fodder in the 60s to 18-20 million hectares, the range of bladder smut expanded. The disease began to be noted in the Moscow (up to 30%) and Leningrad (single) regions, it was also registered in Tataria and Bashkortostan, Pskov, Novgorod, Kaliningrad, Ryazan, Yaroslavl, Gorky, Kirov, Chelyabinsk, Omsk, Novosibirsk regions, in the northern regions of the Far East East (Kalashnikov, Shapiro, 1962).
The prevalence and severity of the disease varies greatly depending on the resistance of the plants, the agricultural technology used and climatic conditions. Infection of various organs (especially the shoot apex) in the early stages of organogenesis is generally more harmful than infection of the stem during the period of protrusion of panicles or unformed cobs. However, when cobs are infected, the largest galls (up to 15 cm) can form, leading to plant infertility (Voitovich, 1958; Kobeleva, Blyandur, 1977, etc.).
It has been established (Nemlienko, 1957) that with natural damage to plants, large galls reduce the yield on average by no less than 60%, medium-sized galls - by 25%, small swellings - by 10%. According to data obtained in the USA (Immer, Christensen, 1928), and later in the south of Ukraine (Klyuchko et al., 1976), the average severity of the disease is 25.0-26.5 and 20.3%, respectively.
U. maydis affects only corn and its closest relatives - teosinte species ( Euchlaena mexicana, E. perennis), not growing in Russia, which allows us to consider the process of accumulation and preservation of infection solely in connection with variety resistance, cultivation technology and protection of corn.
One of the reasons for the appearance of this article is the need to clarify the terminology and characterize the contribution of certain protection methods to improving the phytosanitary situation in corn crops. Unfortunately, erroneous recommendations regarding the development of the epiphytotic situation of bladder smut on corn are still sometimes published (Table 1).
Table 1. Excerpts from scientific, educational, popular science literature and recommendations on plant protection
| Link | |
|---|---|
Plants are infected throughout the growing season. | |
Their highest susceptibility to the disease is observed in the period from panicle ejection to milky ripeness. During the growing season of corn, the fungus can produce 3–5 generations, which explains the strong manifestation of the disease at the beginning of harvesting. | |
Infection of corn can also occur during seed germination. In the case of a seedling disease, this disease is especially harmful, since a general infection of the entire plant occurs. | |
Spraying corn with Bayleton fungicide, 25% pp. - 0.5 kg/ha in the flowering phase of the cobs against blister smut, root rot and fusarium. | |
A single treatment of corn crops (in the phase of ejection of cob threads) with triadimefon-based fungicides at a working fluid consumption rate of 300 l/ha reduces the number of plants affected by bladder smut, helminthosporium, rot of cobs and stems, and fusarium. | |
Treating seeds only solves the problem of seed infection, because infection is possible in later phases | |
General damage to plants may also occur if the infection penetrates the plant during the germination phase. During the growing season, the fungus can produce three to four, and sometimes five generations, which explains the strong manifestation of the disease at the beginning of corn harvest. |
The main goal of the work is to critically examine the prevailing ideas in phytopathology and rethink the main provisions of the existing paradigm, taking into account literature data and the author’s own materials. To achieve this goal, first we will briefly consider bioecology U. maydis and the specifics of the relationship between the fungus and the plant that feeds it.
Results and discussion
Numerous studies have been devoted to the etiology of bladder smut, the beginning of which dates back to the last quarter of the 19th century (Breffeld, 1895; Hitchcock, Norton, 1896), and their intensification - to the first half of the 20th century, when the biology, physiological specialization and nature of corn resistance to U. maydis(Garber, Quisenberry, 1925; Immer, 1927; Christensen, 1930).
U. maydis- a tetrapolar species with multiple tetrapolar heterothallism, in which plant infection and completion of the fungal development cycle are caused only by sporidia that differ simultaneously in the “a” and “b” alleles (Rowell and De Vay, 1954; Holiday, 1961). Shows a low level of differentiation of populations U. maydis in relation to the mating type b locus, which does not exclude a model of neutral evolution (Zambino et al., 1997).
Many years of research have proven the instability of physiological races U. maydis, due to its strong variability in morphological, cultural characteristics and pathogenicity (Stakman, Tyler, Hafstad et al., 1935; Kuznetsov, 1963; Karatygin, 1968). New biotypes (and their compatible pairs - myxobiotypes) of the fungus can arise as a result of mutations in the haploid, diploid and dikaryotic phases (Karatygin, 1969).
The presence of a genetic system of sexual incompatibility of mycelium from sporidia of the same mating type prevents inbreeding in the pathogen population, thereby ensuring the maintenance of its high heterogeneity (Kuznetsov, 1963; Salunskaya, 1969; Barnes et al., 2004).
Wide variation in a variety of traits, including virulence, characterizes the uniqueness of U. maydis among smut fungi, the extreme plasticity of its genetic system. These characteristics, along with the enormous fertility of the fungus and the instability of its physiological races, initially caused methodological difficulties in breeding for resistance to the pathogen, as well as in the implementation of protective measures.
U. maydis refers to heat-loving species, the teliospores of which begin to germinate at 0-5° C and do not germinate above 35° C (Hutting, 1931). After 4 years of storage of teliospores in laboratory conditions, 24% of them retained their germination, but with natural spraying during the harvesting period, they lost their germination by 75% by the beginning of summer. The death of teliospores occurs only after sufficient moisture and increases with the depth of embedding in the soil. It has been shown that in the central zone of the Russian Federation, teliospores persist in the soil for more than 11 months (Kuznetsov, 1963), and in galls - up to 2 years or more.
The optimum for gall formation is 20-25° C (Schmitt, 1940). Freshly ripened teliospores germinate easily, but after 1-2 months their germination rate decreases, often up to 50% (Nemlienko, 1957).
Teliospores do not lose their germination after passing through the digestive tract of animals. They are carried over long distances along with dust, usually germinate in places of accumulation in the presence of moisture (precipitation, dew): initially in the funnel of the leaves, after flowering - in the axils of the leaves, and after night dew - on other parts of the corn. The onset of hot, dry weather is especially favorable for the germination of teliospores, sporidia and for penetration into the integumentary tissue of the plant (Corn smut Ustilago maydis. Cornell Univ., Dept. of Plant Pathology and Plant-Microbe Biol.).
It was reported (Borggardt, 1932; Ulyanishchev, 1952) that insects can transfer teliospores of bladder smut from plant to plant. Thus, the life cycle of larvae is associated with growths of corn smut and smut of weedy millet grasses. Phalaerus politus feeding on fungal spores U. maydis(Boving, Graighead, 1931).
According to O. Walter (1934), infection U. maydis occurs through the introduction of an infectious hypha formed from sporidia or directly from a teliospore, with the second variant of penetration being more widespread. This fact, as noted by F.E. Nemlienko (1957), is of great interest, since the fungus can get by with a minimum of moisture, which might not be enough for the formation of basidiospores, but which is sufficient for the germination of teliospores. It has been established that the prevalence of smut, taken into account once based on its visible manifestations, must be supplemented by repeated counts during the ripening period (Davis, 1936), since many lesions of the lower cobs are not visible due to their covering with wrappers. The presented original data on a 2-3-fold increase in the number of affected plants with age can serve as an indicator of the presence of infection in a latent state and the possibility of its manifestation in the form of galls on stem nodes.
Extensive information about the reasons for the periodic increase in the spread of the disease can be reduced to three main points: embedding smut galls into the soil reduces the incidence of the disease and the degree of damage to plants; in dry and rainy seasons, the prevalence of the disease is lower, its increase is associated with frequent changes in dry conditions and short-term precipitation; Injuries caused by tillage implements, insects (Swedge flies, corn borer, bollworm), birds and hail increase the prevalence of smut.
Table 2. Main factors that can influence the development of corn smut
| Object and nature of influence | Cause | Result | A source of information |
|
|---|---|---|---|---|
| Agricultural technology, cultivation technology | ||||
A sharp change in the supply of moisture to plants | Disturbs the normal course of physiological processes | Weakens plant resistance to disease and creates | Increasing susceptibility | Nemlienko, 1957 |
Organic fertilizers that remain unplowed into the soil; richly fertilized soil | Preservation of the infectious onset in the autumn-winter period | Increased infectious background; lengthening the period of dispersal and germination of plants | Contribute to the spread of disease | |
| Environmental factors | ||||
The amount of precipitation during the period of panicle extension is the milky ripeness of the grain; dry, windy weather in late spring - early summer | Better germination of teliospores, budding of sporidia | Improving conditions for infection | Kobeleva, Blyandur, 1977; Jugenheimer (1979) |
|
| Anthropogenic impacts (agricultural tools, hybridization technologies) | ||||
Herbicides | Plant metabolism disorder | The occurrence of pathologies of growth and development in violation of the regulations for use | Increased spread of disease | Jugenheimer, 1979; Ivashchenko, 1983; Cabanettes, 1986; Dudka et al., 1988 |
| Insects, birds | ||||
Phalaerus politus | Feeding on teliospores, their transfer; transfer of teliospores, and contamination of plants during feeding | Feeding on U. maydis teliospores; Injuries, transmission of infection, contamination | Increased spread and extent of damage | Boving, Graighead, 1931; Borghardt, 1932; Ulyanishchev, 1952; Ivashchenko, 1992; Ivashchenko, Sotchenko, 2002 |
It is known that during the onset of drought (and with frequent alternation between periods of moisture and dry ones), the turgor of the tissues of the leaf funnel decreases (as a manifestation of structural immunity, which contributes to the spread of the infectious principle that formed earlier during the period of sufficient moisture). It was also found that variations in weather conditions are statistically significantly associated with late embryonic mortality of corn borer eggs. It decreases significantly during the development of the first generation under conditions of high air humidity (r = -0.77), and the second - with increased air humidity (r = -0.71) and increased precipitation (r = -0.85). Early embryonic mortality of eggs of the second generation was also associated with air humidity (r = -0.90) and the amount of precipitation (Frolov, Malysh, 2004).
The influence of moisture is multifaceted, but the analysis of simple relationships leads only to a statement, less often - to the identification of a trend, while when analyzing the interactions of pathogens and phytophages - to obtaining final, clearly visible results, assessed in terms of harmfulness. In the list of factors considered, agrotechnological methods of cultivating plants are required, but only wound infections are largely controlled, which requires a comparative consideration of the relationships both in the plant-host-pathogen system and in the plant-host-phytophage-pathogen system in order to identify key links, determining the greatest effectiveness in containing the spread of the disease, its development and harmfulness.
I. Relationships in the plant-host-pathogen system
Penetration U. maydis.
According to O. Walter (1934), infection occurs through the introduction of infectious hyphae formed from sporidia or directly from teliospores, and the second variant of penetration is more widespread.
The hypha that penetrates the cell forms a thin thread-like mycelium. The fusion of thin hyphae from two different-sex individuals (+ and –) gives rise to the formation of binucleate thick nodular intracellular hyphae that penetrate cells in different directions (Mundkur, 1949). Sporidia, as noted by I.V. Karatygin (1981), germinate with insignificant primary mycelium, usually spreading only in the epidermal cells of the infected plant. Hyphae from germinating teliospores are thicker (3-4 µm) than sporidia (2-3 µm); they spread along the surface of the cuticle to a distance of 90-110 µm or more before the formation of appressoria and the subsequent introduction of fungal mycelium into corn tissue, and it occurs without clearly defined specialization by cell type, and the mycelium can spread over a short distance towards meristematic tissues. These are meristems of lateral vegetative buds and adventitious roots, rudimentary ears, intercalary meristem of axial organs, stem apex cells, leaf meristems, floral meristems, in particular meristems of developing grains, as well as the zone of intercalary leaf growth. Infection under natural conditions is usually carried out by several germinating teliospores located on the surface of poorly differentiated tissues. In this case, one part of the teliospores germinates with the formation of dikaryotic mycelium, the other with the formation of sporidia. Anastomoses are common between dikaryotic mycelia (Karatygin, 1968; Mills and Kotze, 1981).
Colonization.
Features of corn colonization U. maydis described in sufficient detail (Davis, 1936). It has been shown that corn is susceptible to infection from the period of formation of the first leaf until the formation of pollen in the anthers, that is, in the presence of meristems accessible to infection. When susceptible varieties are artificially infected, the pathogen is able to penetrate the cells of the root cortex, but locally, and is detected only by microscopy (Sabbagh et al., 2006). The pathogen invades mainly through developing generative organs, buds, and young leaves, but is unable to infect a seedling through an intact coleoptile, so under natural conditions, seedling damage by the pathogen is extremely rare. Infection often occurs at the “leaf rosette” stage, when the plant reaches a height of 30-100 cm. G. Davis (1936) believes that when the ears are infected, spores penetrate between loosely pressed leaf wrappers at the beginning of the pollination process, but the mycelium does not penetrate through the stigmas . Corn is most susceptible 10-14 days before panicle extension, when the growth cone meristems are most open and accessible to infection. These features of the place and method of infection of corn distinguish U. maydis from other smut fungi. Usually, on a plant that has a smut gall, it is possible to detect mycelium in various areas, which is a consequence of repeated infection of the plant during its ontogenesis. The nature of the distribution of the fungal mycelium throughout the plant can be assessed as multi-local, and the mycelium is able to remain latent in the axillary buds.
Mycelium distribution data U. maydis in corn tissues are given in a number of monographs (Nemlienko, 1957; Christensen, 1963; Karatygin, 1981) and numerous publications. The vast majority of researchers consider blister smut to be a typically local disease, and descriptions of “total” infection of seedlings, “cords” on leaf veins and other symptoms are a consequence of a primary multiple infection.
Hallogenesis.
The structure of pathologically altered tissues of corn affected by U. maydis, was studied in connection with the previously existing point of view that the mycelium of the fungus does not cause changes in the first stage of plant life, only with age nodules appear and rapidly progress due to the hyperplastic and hypertrophic action of the mycelium of the fungus. Pathohistological studies (Davis, 1936) have established that in the newly formed groups of young cells appearing in the peripheral zone of the main parenchyma of stems and leaves, there is no mycelium. The gall grows due to the formation of new groups of very young cells with a thin cell wall and an abundance of protoplasm. After some time, mycelium is formed, which permeates the entire gall tissue. The nature of mycelium growth in galls differs from that in morphologically normal tissues in that large clusters of it are formed. Subsequently, the hyphae are segmented, and teliospores are formed from individual segments.
The works of I.V. Karatygin (1971, 1981) showed that sporogenic mycelium accumulates, as a rule, in the intercellular spaces of infected tissues, where the formation of sori begins. It has been established (Davis, 1936) that apparently healthy plants can often be infected in one or many places and produce galls only under certain conditions, in many cases showing no signs of disease at all. This has been confirmed by other researchers (Mikhalevskaya, 1967; Karatygin, 1981).
Studies of the problem of galogenesis have led to the conclusion that the rate of growth of swellings depends on the location, weather conditions and, possibly, the degree of resistance of the host plant (Scurti, 1950; Christensen, 1963). The swellings grow most quickly on the cobs, where their growth, especially before ripening, can reach 4 cm in diameter per day. Swellings on leaves and panicles increase in size much more slowly (Nemlienko, 1957).
A characteristic feature of the pathogenesis of the disease is an increase in transpiration and a decrease in the sugar content in the stem with damage to various organs (Hard-Karrer, 1926; Sidenko, Sotula, 1975). At the same time, due to a doubling of the rate of accumulation of dry matter in pathologically growing tissues, a smaller number of leaf primordia are formed on the growth cone of the stem, and the growth of the latter is suppressed (Mikhalevskaya, 1975).
Features of the manifestation of the disease.
That corn is most susceptible to U. maydis when its height reaches a foot (30.5 cm), it is also known from the works of O. Brefeld (Brefeld, 1895) and other authors (Clinton, Hitchcock, Norton, 1896; Platz, 1929). O.A.Platz (1929) showed that galls on stem nodes rarely appear on corn in the first 70-80 days from sowing or 40 days after the differentiation stage. Most often, plants begin to be affected approximately 40-45 days after germination, that is, 20-25 days before the panicles appear.
In experiments with artificial infection of corn U. maydis F.E. Nemlienko (157) noted that a smut spot visible to the naked eye is formed after 8-12 days, and a mature swelling with completely viable spores - after 20-24 days. Similar results were obtained by other authors, who noted the first symptoms of the disease after 2-3 weeks, and the duration of the period from the beginning of the formation of galls to the maturation of spores in them - from 7-15 days to 2-3 weeks (Karatygin, 1971; Slepyan, Karatygin, 1973, 1976). It was shown that when three-day-old seedlings were inoculated (by the vacuum method), galls appeared on leaves and stems on days 5-7 after infection (Mikhalevskaya, 1967).
I.V. Karatygin (1981) noted that mature teliospores are capable of germinating and causing a new infection, but believed that in the conditions of most of the territory of the former USSR the significance of this secondary infection is small.
Thus, depending on the time and method of penetration of the fungus (introduction of infectious hyphae, introduction of teliospores, sporidia during inoculation, contamination due to damage to corn tissue), the latent period can last from 7 to 70 days. In this regard, we should quote the assumption of F.E. Nemlienko (1957) that with artificial infection “the fungus on a plant can go through up to 3-4 passages during the growing season,” which was often taken as an axiom, especially by representatives of companies selling pesticides, who recommended treating smut during the flowering period of corn (see. Table 1).
Corn resistance to U. maydis and principles of selection.
The nature of corn resistance to smut has been studied by phytopathologists, physiologists, biochemists, breeders and geneticists. The earliest classification, proposed by M. Middendorf (1958), included three forms of resistance:
Subsequently, F.E. Nemlienko, I.E. Sidenko (1969) combined the first and second forms under the name “structural” (“mechanical”) resistance, for the third they retained the name physiological resistance, proposing to identify structural resistance against natural and provocative backgrounds, and physiological resistance through the artificial introduction of teliospores into tissues capable of infection . In addition, it was proposed to take into account the manifestations of age-related and organotropic resistance (Salunskaya, 1962; Nemlienko, Kulik, 1962; Nemlienko, Sidenko, 1967; Geshele, Ivashchenko, 1973). These methodological approaches are widely used in breeding institutions in Russia (and previously in the USSR).
A comparative study of several previously proposed inoculation methods (Chekalin, 1961; Nemlienko, Sidenko, 1967; Nemlienko et al., 1969) led us to the conclusion: 1) organotropic manifestations of resistance in lines are not correlated; 2) 100% damage to the ears, achieved in samples inoculated on days 2-3, and the manifestation of differences on the 7th day after the appearance of stigmas (as proposed by the All-Russian Research Institute of Corn, 1980) are only evidence of a different duration of the period of susceptibility (Ivashchenko, 1992) .
It is important to note that the incidence of cobs reaches 100% in material that has undergone long-term study under negative selection. It has been shown that injection into the cob leads to a 4-7-fold (Chernobay, 1986; Ivashchenko, 1992) increase in infestation, and many authors note a predominant discrepancy between the indicators of general and physiological resistance, that is, the incomparability of data obtained on natural and artificial backgrounds.
Works of the second half of the twentieth century expanded ideas about biology U. maydis, etiology and pathogenesis of the disease, methodological principles of selection for resistance and ways of protection against the pathogen (Stakman, Christensen, 1953; Nemlienko, 1957; Kuznetsov, 1963; Christensen, 1963). Further studies of the biology and genetic structure of populations confirmed the instability of the physiological races of the fungus, due to strong variability in morphological, cultural characteristics and pathogenicity (Stakman, Tyler, Hafstad et al., 1935; Kuznetsov, 1963; Karatygin, 1968, 1981; Yurku, Lazu, 1987 ).
The establishment of heterozygosity of varieties for resistance genes (Garber, Quisenberry, 1925) and the polygenic nature of structural and physiological resistance (Immer, 1927; Munteanu et al., 1969; Bojanowski, 1969) was used to obtain resistant lines by inbreeding varieties and populations, as well as to integrate lines with different types of resistance in the hybrid genotype. Taking into account these biological features, selection for a race-specific type of resistance was considered inappropriate, which made it possible to avoid further devaluation of the source material and ensured long-term resistance of the selected lines and hybrids to various ecological populations of the pathogen (Russell, 1982). Thus, a number of American corn lines resistant to U. maydis in the USA, showed stability in the south of Ukraine (Ivashchenko, 1977).
It is known that infection is limited by structural (mechanical) barriers (tight covering of the growth cone by a leaf tube, tight fit of the leaf sheaths of the stem, good covering of the cob with a wrapper), turgor state of tissues, shortened receptivity phase of individual organs, resistance to damage by insects, phytoncidity of tissues and the manifestation of active physiological reactions of a protective nature. To this list of protective features it should be added that only young tissues are susceptible, i.e. there is age-related stability.
It has been shown (Geschele, Ivashchenko, 1973) that the genetics of resistance, as a complex trait, must be studied differentially according to the manifestation of each protective mechanism separately. At the same time, information about the susceptibility of corn U. maydis(Jones, 1918; Immer, Christensen, 1931, 1942; Nemlienko, 1957; Chekalin, 1961; Nemlienko, Kulik, 1965; Vozdova, 1965; Ryumina, 1970, etc.), obtained on the basis of natural damage, characterizes the action of many factors ( including those of unknown nature). When artificially infecting an ear or leaf funnel, the role and inheritance of only a few protective mechanisms are assessed.
II. Relationships in the plant-host - phytophages - pathogen system
A number of authors, noting the dependence of the development of the disease on many factors, include Swedish flies and corn borer among them (Jenkins, 1929; Chernetskaya, 1932; Haenseller, Papper, 1944; Christensen, Schneider, 1950; Pavlov, Kozhevnikova, 1957; Koehler, 1959 ; Yakovleva, 1963; Susidko, Bienko, 1966; Ryumina, 1972; Blyandur, 1977), however, they consider damage to corn by insects as a temporary and concomitant factor, without taking into account the type of damage, connection with ontogenesis and the nature of the relationship between pests and the plant.
Research results in recent decades have shown that “entomologists and mycologists have become unexpectedly complementary; a partial overlap of interests in the field of scientific research was discovered, and the need and promise of interdisciplinary approaches arose” (Wheeler, Blackwell, 1984). For example, the life cycle of larvae is associated with growths of corn smut and smut of weedy millet grasses. Phalaerus politus feeding on fungal spores U. maydis(Boving, Graighead, 1931). Further studies established the role of entomofauna not only as pests that open the gates of infection for fungal and bacterial flora, but also as carriers of corn diseases: root and stem nematodes - in the development of root and stem rots and dwarf mosaic (Palmer, 1969; Smiljakovich et al. , 1975; Goswami, Raychaudhuri, 1978); Swedish flies - bubble smut (Pavlov, 1956; Nemlienko, 1957; Shapiro, 1961); corn borer - bladder smut, stem rot, ear diseases (Christensen et al., 1950; Koehler, 1950); leaf beetles (D iabrotica virgifera, D. longicornis) – root rot and fusarium cob (Palmer, Kommedahl, 1969; Gilbertson et al., 1986). In turn, the dwarf mosaic virus increases the susceptibility of seedlings to gibberellosis and helminthosporium root rot (Tu, Ford, 1971), and adult plants to smut (Ivanovic, 1978).
The first pathogenic associations - between the causative agent of elm graphiosis and the bark beetle, discovered in Europe (Spierenberg, 1922), and between woolly aphids and the causative agent of apple canker in the USA (Leach, 1940, cited from Anderson et al., 1984) - allowed rethink not only the etiology of diseases, but also their control. Subsequently, many domestic and foreign researchers noted an increase in the prevalence of bubbly smut in years with high numbers of Swedish flies (Pavlov, 1955; Nemlienko, 1957; Pan Xiong-Fei, 1959; Shapiro, 1961; Fedin, 1962; Pavlov, Kozhevnikova, 1964; Shkurpela , 1965; Jugenheimer, 1979, etc.), considering wound infections as an additional factor, as a consequence of Swedish fly larvae overcoming the growth barrier created by growing leaves. In this regard, it is advisable to consider the scheme developed by I.D. Shapiro (1985) and the features of the pest’s penetration into the plant. As the author notes, “Swedish fly larvae are adapted to living inside a plant and use meristems for food. After hatching, they immediately move to the growth cone, overcoming a barrier of not yet formed leaves that tightly fit the apex. The importance of the growth barrier in corn is most pronounced. The reason for this is the continued growth of the upper leaves surrounding the growth cone. For example, the growth rates of the 4th leaf in the Odesskaya 10 variety and the mid-early Mandorfer and Voronezhskaya 80 are close and reach 1.05-1.10 mm/h, and in the early-ripening Beloyaroye millet variety - 0.5 mm/h. In the variety Voronezhskaya 80, the most resistant to Swedish flies, the larvae must penetrate to the growth cone through 14 layers of leaves along the long path and through 10 along the short path (Fig. 1). Only a few larvae that develop on corn manage to move to the growth cone and stop the growth of leaves 1 and 2.”
It is important to note that the penetration of Swedish fly larvae and the infectious beginnings of smut into the meristem tissues of corn is a general genetically predetermined need for nutrition by tissues rich in protein and carbohydrates, a condition for their successful growth and development.
The path of penetration of teliospores or sporidia in the absence of wound channels that we are considering (Fig. 1, path 1) is probably rarely successful, given the low rate of colonization of leaf tissues by the fungus and the rapid removal (12-25 mm/day) of damage zones (and infected zones) to the periphery of the leaf funnel.
Our assessment of the resistance of 101 corn hybrids to the Swedish fly showed that with the degree of plant damage from 10 to 56% (on average 26.6%), a weak negative relationship (r = -0.25, P‹0.05) appears between the damage intensity indicators and the degree of plant damage .
With an average damage of hybrids of 26.6%, the degree of their damage by bubbly smut was 2.26%, which confirms the data of I.D. Shapiro (1985) that “only a few larvae developed on corn manage to move to the growth cone and stop the growth of leaves 1 and 2,” as well as our assumption of the low probability of successful infection by the fungus in the absence of damage by the Swedish fly.
The results of a sequential assessment of the damage of 101 hybrids by the Swedish fly and the corn borer are shown in Table 3.
Table 3. Dynamics of manifestation and localization of galls U. maydis in the ontogenesis of corn under conditions of natural invasive and infectious backgrounds
Organs affected | Phytophagous | Proportion of organs revealed by surveys of corn damage at different stages of organogenesis, % | ||||
|---|---|---|---|---|---|---|
Individual leaves, or a group of them (diffusely), with the manifestation of “saber-likeness” or dwarfism of plants | ||||||
Bottom of stems | ||||||
Stems in the middle part and under the cob | ||||||
Stems above the cob, panicles | ||||||
Basic cobs | ||||||
Vestigial cobs | ||||||
Note. Stages of organogenesis: IV-VII - leaf funnel; VIII - extension of panicles; IX - flowering; X - milky ripeness; XII - complete ripeness of the grain. ШМ - Swedish fly; KM 1 and KM 2 - corn borer of the first and second generation in the season, respectively.
As can be seen from the data in Table 3, the manifestation of smut in plants damaged by the Swedish fly begins in the early leaf funnel phase and ends at the beginning of panicle extension. During the period of panicle development, the appearance of smut begins on plants damaged primarily by the first generation of corn borer, and from the period of flowering to ripening - by the second generation. Damage by the cotton bollworm leads to the development of smut on the cobs into milky - full ripeness of the grain. The sequence and extension of the summer of these pests and the damage caused to plants also determine the long period of manifestation of smut, as a result of which the impression of development of several generations is created U. maydis.
Our long-term studies (350 lines and hybrids, 1985-1988) revealed a highly reliable connection between the development of bubbly smut and ear diseases with corn borer damage in an area with one generation of the pest (forest-steppe of Ukraine) and with two (Krasnodar Territory). In the Cherkasy region, these correlations were 0.73 - 0.98 for bladder smut and 0.79 - 0.94 for fusarium cob in 1985-1988, then in the Krasnodar Territory - 0.89 - 0.91 for the same period ( Ivashchenko, 1992; Ivashchenko et al., 2000).
The presence of drill flour and visible damage facilitates the establishment of a relationship between corn borer damage and smut damage, since the source of the disease is predominantly local. During a remote superficial examination, establishing such a connection is difficult due to extensive pathological degeneration of tissues (the cob is damaged completely or partially), but even in this case, traces of damage to the stalk of the cob, its stem or wrappers, stem, and panicle remain. It is easier to establish such a connection when corn is damaged by the cotton bollworm due to larger damage zones.
Inclusion U. maydis into the tritroph system (corn-phytophage-entomophage) is illegal, since the pathogen does not have a consort relationship with the corn borer and cotton bollworm. However, the creation of wound surfaces (which is annual and sustainable) serves as a kind of edificator of environment-forming conditions that facilitate colonization of susceptible meristems by the fungus.
One of the negative consequences of weed control could be an increase in the incidence of bladder smut when using atrazine and lasso/atrazine (Dudka et al., 1988). More severe damage to corn plants by bladder smut on a herbicide background than on a fertilized one was noted in the southeast of the central Chernozem region (Laptiev, 2008). The experience of plant protection in France also deserves attention (Cabanettes, 1986), where bubbly smut reached alarming levels when using a number of pesticide mixtures.
Plant infection U. maydis The breaking off of panicles in areas of hybridization also contributes, as a result of which the infestation of plants of the maternal form increases on average by one and a half times, reaching 20% in susceptible lines (Ivashchenko, 1983). This elimination of structural stability leads to a greater manifestation of physiological stability. Thus, we identified line V 312 with physiological type resistance (the size of the smut swelling does not exceed 2-3 cm), as well as lines with structural and physiological resistance simultaneously (A632, B37). According to R.U. Jugenheimer (1979), breaking off panicles in areas of hybridization, lack of pollination of ears and damage to plants by hail are the main reasons for the increase in infestation U. maydis. As the main reason explaining the increase in the incidence of smut on unpollinated cobs, it is necessary to indicate the eating of the stigmas of the cobs by cotton bollworm caterpillars, which leads to an extension of the period of receptivity of their embryonic meristems.
Our research on the role of seed contamination by teliospores U. maydis(Sotchenko et al., 2008) confirmed the previously accumulated experience of plant protection and led to the conclusion that it is inappropriate to search and use special disinfectants for protection against bubbly smut, since the disease is not transmitted by seeds and does not affect underground organs (roots and mesocotyl), although the penetration of the fungus into the roots has been experimentally proven (Sabbagh et al., 2006).
Conclusion
The complexity of the nature of field resistance to the disease, the difficulty of creating universal infectious backgrounds and the need for many years of studying breeding material in various environmental conditions led to the conclusion that field resistance to the bubbly smut pathogen is divided into structural and physiological. Methods of artificial infection of corn U. maydis unjustifiably widespread in the system of research institutes and State variety testing due to the ability to obtain with their help a high level of damage to stems and ears, practically not observed in nature, since negative selection makes it possible to cull susceptible forms during the selection of source material and many years of testing. Elimination of structural stability of cobs during screening, even with the introduction of a suspension U. maydis into the area above the panicle and ear without damaging them, led to the identification of samples with physiological resistance (with a minimum size of galls). At the same time, differences in the prevalence of the disease, due to the duration of the period of susceptibility, have rarely become adequate to the natural ones associated with the specific damage of plants by a complex of pests. Selectivity as a type of plant resistance to insects and its influence on the reproductive potential of pests, which are taken into account when selecting for group resistance to pests, have escaped the attention of researchers. Of course, the technological advantages in recreating the epiphytotic level of disease development with artificial inoculation are obvious, but the features and degree of expression of structural immunity are sacrificed for manufacturability, which are leveled out with artificial inoculation, narrowing the possibilities of selection. And one of the important tasks of research is to use this natural background of primary differentiation (carried out by phytophages) to identify the least damaged and affected breeding samples.
The above-described features of the relationship in the plant-host - phytophages - pathogen system characterize the monocyclic type of disease, the epiphytotic manifestations of which have not been noted.
The pathogen is not transmitted by seeds; their contamination with teliospores does not lead to the onset of the disease (in contrast to loose smut). Seed dressing protects seedlings from a wide range of pathogens, including the transfer of teliospores U. maydis to new regions. In recent years, the inclusion of fungicides in corn crop protection systems to reduce the incidence of bubbly smut on the cob is rather of a preventive nature, not associated with a predicted and economically calculated crop shortage. Such treatments are probably advisable in the list of methods for protecting sweet corn when the number of cob pests is predicted to be high, where the yield loss from pests and smut is higher than on conventional corn.
The recommendations given in the scientific, educational, popular science and specialized literature of the last decade (similar to those cited in Table 1) are formulated on the basis of insufficiently clear ideas about the etiology of the disease and its pathogenesis.
Associated pathosystem ( Zea mays— pests (Swedish fly, corn borer, cotton bollworm) — U. maydis) is co-evolutionarily established, and in this sense it complements the basic paradigm in relation to practical selection for group and complex resistance to pests; its analysis makes it possible to optimize the development of an ecologized plant protection system from phytophages and pathogens. It is characterized by the manifestation of evolutionarily stable non-race-specific resistance in maize, the preservation of which is ensured by a correctly chosen selection strategy at the beginning of the 20th century. The preservation of this resistance requires broader monitoring of wound damage as an indicator of the primary selection of a certain plant genotype (carried out by phytophages), as a natural background against which it is easier to identify the least damaged and affected selection samples, as a predictable and largely controllable factor in the biologization of the corn protection system.
Literature
Azbukina Z.M. About fungal and bacterial diseases of corn in the Primorsky Territory. // Proceedings of Primorsky Agricultural Institute, 1962, 1, pp. 71-74.
Borggardt A.I. Current state of issues in the field of knowledge of corn diseases. // Selected works on phytopathology. M., 1961, pp. 136-148.
Borisenko S.I. Biological features of corn smut. // Sat. scientific tr. 1951-1953 Kharkov, 1954, pp. 141-149.
Vilkova N.A., Ivashchenko V.G., Frolov A.N. and others // Methodological recommendations for assessing corn for complex resistance to pests and diseases. M., VASKHNIL, 1989, 43 p.
Voitovich K.A. Assessment of the infestation of bubbly smut in breeding materials and corn hybrids. // Proceedings of the Moldavian VIZR station (1956-1958), 1958, 3 p.
Voronin K.E., Vilkova N.A., Afanasenko O.S., Ivashchenko V.G., Issi I.V., Voronina E.G. Integration of plant immunity and biomethod as a biocenological basis for the strategy for improving phytosanitary technologies in agroecosystems. // Bulletin of plant protection, St. Petersburg, 1999, 1, p. 67-73.
Geshele E.E., Ivashchenko V.G. Evaluation of corn in the process of breeding for resistance to infectious diseases. // Sat. scientific works of VSGI, Odessa, 1973, p. 211-225.
Ivashchenko V.G. Results of studying forms resistant to bladder smut in hybridization areas. // Breeding and seed production, 1983, 11, p. 20.
Ivashchenko V.G., Florya M.B., Nikonorenkov V.A., Inglik P.V., Khromenko A.S. Study of corn resistance to various environmental populations of stem rot and blister smut pathogens. // Proceedings of the II National Symposium on Plant Immunity, Plovdiv, 1983, 1, p. 243-249.
Ivashchenko V.G. Fungal diseases of corn stems and leaves in various ecological and geographical zones. // Mycology and phytopathology, 1991, 25, 5, p. 432-437.
Ivashchenko V.G. Corn cob diseases. // Plant protection, 1991, 2, pp. 18-20.
Ivashchenko V.G. Resistance of corn to major diseases and development of methods for increasing it. // Author's abstract. doc. diss. St. Petersburg, 1992, 38 p.
Ivashchenko V.G. The harmfulness of the main diseases and the corn borer and the possibility of reducing it. // Corn and sorghum. 1996, 3, pp. 12-15.
Ivashchenko V.G. Types of corn resistance to diseases and ways of their use in breeding practice. // Mater. scientific seminar “Types of plant resistance to diseases”, St. Petersburg, VIZR, 2003, pp. 61-82.
Ivashchenko V.G. Prevalence of major corn diseases in Russia and the CIS. // Bulletin of plant protection (Appendix), St. Petersburg, 2007, pp. 68-81.
Ivashchenko V.G., Frolov A.N., Sotchenko V.S., Garkushka V.G. Breeding corn for resistance to pests at the present stage of agricultural production in Russia. // Bulletin of plant protection, 2000, 2, p. 20-25.
Ivashchenko V.G., Sotchenko E.F. Fusarium disease of corn cobs in the Stavropol region: etiology of the disease, variety resistance. //Matter. scientific-practical conf. “Breeding, seed production, corn grain production, 2002” Pyatigorsk, p. 157-164.
Ivashchenko V.G., Frolov A.N., Dubrovina A.G., Garkushka V.G. Corn resistance to pests as the most important reserve for realizing high productivity potential in breeding for heterosis. //Doc. IV International Congress “Grain and Bread of Russia”, November 11-13, 2008, St. Petersburg, 2008, p.46-48.
Kalashnikov K.Ya., Shapiro I.D. Pests and diseases of corn. M.-L., Selkhozgiz, 1962, 189 p.
Karatygin I.V. Smut fungi: ontogeny and phylogeny. L., 1981, 202 p.
Karatygin I.V. The structure of the pathogen and its development in the tissues of host plants as a criterion for plant resistance to fungal infection. // Mycology and phytopathology, 1968, 2, 5, pp. 414-420.
Karatygin I.V. Formation of sori and differentiation of spores Ustilago maydis(DC.) Cda. on the leaves. //Doc. Academy of Sciences of the USSR, 1968, 183, 6, pp. 1458-1460.
Karatygin I.V. Genetic characteristics of the development cycle Ustilago maydis(DC.) Cda. // Mycology and phytopathology, 1969, 3, 4, p. 368-376.
Karatygin I.V. Development in tissues Zea mays L. blistering smut pathogen in connection with its life cycle. // Author's abstract. Ph.D. diss., L., 1971, 25 p.
Karatygin I.V. Genetics of smut fungi.//Genetic bases of plant resistance to diseases. L., Kolos, 1977, p. 95-109.
Klyuchko P.F., Ivashchenko V.G., Sergeev V.V. Using the method of sister crossings in the selection of corn for resistance to bladder smut. // Scientific and technical. bulletin VSGI, Odessa, 1976, 27, pp. 10-13.
Kobeleva E.N., Blyandur O.V. Selection of mutant maize lines for disease resistance. Chisinau, 1977, p.67.
Kuznetsov L.V. About the viability of the mushroom Ustilago zeae(Beckm) Ung. - the causative agent of corn smut. // Vestn. Moscow state University, VI, Biol. and soil., 1963, 2, pp. 30-39.
Kulik.T.A. The influence of environmental factors on the susceptibility of corn to bubbly smut ( Ustilago maydis(DC.) Cda.). // Mycology and phytopathology, 1968, 2, 5, pp. 428-432.
Laptiev A.B. Bioecological justification for phytosanitary optimization of agroecosystems in the southeast of the central Chernozem region. //Author. doc. dis. St. Petersburg, 2008, 39 p.
Levada S.A. Increasing the effectiveness of protective measures against corn diseases in irrigated areas of the steppe of the Ukrainian SSR. // Author's abstract. Ph.D. diss. Dnepropetrovsk, 1990, 22 p.
Meshcheryakova R.I. Increasing the resistance of corn to bladder smut. // Author's abstract. Ph.D. diss. Kharkov, 1959.
Musiyko A.S., Geshele E.E., Walter O.Yu. On some issues of the biology of the causative agent of corn smut. //Agrobiology, 1969, pp.579-582.
Nemlienko F.E. Corn diseases. Selkhozgiz, 1957, 230 p.
Nemlienko F.E., Sidenko I.E. Ontogenetic resistance of corn to bladder smut. // Dokl. VASKHNIL, 1967, 1, pp. 7-9.
Nemlienko F.E., Grisenko G.V., Kulik T.A., Sidenko I.E. On the immunity of corn to smut and stem rot. // Bulletin. All-Russian Research Institute of Corn. Dnepropetrovsk, 1969, 1(3), pp.49-54.
Nemlienko F.E., Sidenko I.E. On the mechanical and physiological immunity of corn to bladder smut. // Proceedings of Kharkov agricultural. Institute, 1969, 79, pp. 67-72.
Nemlienko F.E. Towards a method for accounting for the infestation of corn by bladder smut // Breeding and seed production, 1949, 4, pp. 68-70.
Nemlienko F.E. The degree of knowledge and practical use of corn immunity to diseases. // Abstract. III All-Union meeting on plant immunity. Chisinau, 1959, pp. 3-8.
Nemlienko F.E., Kulik T.A. Organotropic resistance of corn to bladder smut. // Corn, 1962, 4, pp. 57-59.
Nemlienko F.E., Kulik T.A. Use of corn resistance to bladder smut in breeding work. // Abstract. report IV All. meeting on immunity agricultural plants. Chisinau, 1965, pp. 181-182.
Nemlienko F.E., Sidenko I.E. Ontogenetic resistance of corn to bladder smut. // Dokl. VASKHNIL, 1967, 12, pp. 7-9.
Pavlov I.F. Methods of controlling Swedish fly and other pests of corn. // In the book: Corn in 1955, Selkhozgiz, 1956, 2, p. 124-127.
Pavlov I.F., Kozhevnikova L.I. Protection of plants from pests and diseases. In the book: Row-crop farming system. M., 1964, pp. 107-120.
Pan Xiong-Fei. Swedish fly and smut on corn. // Protection of plants from pests and diseases, 1959, 2, p.25.
Pikovsky M., Kirik N., Verdysh A.. Diseases of corn seeds.// Vegetable growing (Ukrainian magazine for professionals), 2010, 12. p.64-67.
Russell G.E. Plant selection for resistance to pests and diseases. M., Kolos, 1982, 421 p.
Ryumina M.A. Resistance of corn to bladder smut and development of methods for its increase. // Author's abstract. Ph.D. diss., L., 1970, 23 p.
Ryumina M.A. Assessment of resistance of self-pollinated corn lines to bladder smut. // Tr. in applied botany, genetics and selection. L., 1972, 46, 3, pp. 91-97.
Salunskaya N.I. Which organs of corn are affected by blister smut? // Botanical Journal, 1964, 49, 7-12, p. 1034-1035.
Salunskaya H.I. Minimality of fungal populations Ustilago zeae(Beckm.) Ung. - zbudnik fluffy soot kukuruji. // Zakhist Roslin, 1969, 7, pp. 41-51.
Slepyan E.O., Karatygin I.V. Productive necrotizing erythroderma is the primary symptom of infection Ustilago maydis(DC..) Cda. on the leaves. // Dokl. Academy of Sciences of the USSR, 1968, 178, 5, pp. 1212-1215.
Slepyan E.I., Karatygin I.V. Order smut (Ustilaginales). // Plant Life, 1976, 2, pp. 346-353.
Sotchenko E.F., Sotchenko Yu.V., Ivashchenko V.G., Alekseeva O.V. The effectiveness of Vitavax 200 FF against dusty and blister smut of corn. // Protection and quarantine of plants, 2008, 2, pp. 27-28.
Susidko P.I. Bienko M.D. Swedish fly in the southern regions and measures to combat it. // Corn, 1966, 10, p. 19.
Tikhonov N.A., Tikhonov S.P. Blister smut of corn in Crimea. // Tr. Crimean state c.-x. experimental station, 1969, 5, p.29-38.
Ulyanishchev V.I. Microflora of Azerbaijan, T.1. Smut mushrooms. Baku, 1952, 334 p.
Uranov A.A., 1935 (quoted from: Vasilevich V.I. Quantitative methods for studying the structure of vegetation: Results of science and technology, In the book: Botanika, M., VINITI, 1972, 1, pp. 7-83.
Fedin M.A. Infestation of corn by Swedish fly and bladder smut depending on sowing time. // Protection of plants from pests and diseases, 1962, 5, p. 29.
Frolov A.N., Malysh Yu.M. Density and mortality of eggs and younger caterpillars of the corn borer on corn plants // Bulletin of plant protection, St. Petersburg VIZR, 2004, 1, p. 42-55.
Chekalin N.M. Evaluation of some methods of infection with bladder smut // Proceedings of graduate students and young researchers of VIR, 1961, 2, pp. 112-116.
Chernetskaya Z.N. Corn diseases. // Summary report of the Gorsk zonal station. Ordzhonikidze, 1932, 22 p.
Shapiro I.D. Swedish fly as a pest of corn. In the book: Distribution of pests and diseases of agricultural crops in the RSFSR in I960 and forecast of their appearance in 1961, L., 1961, pp. 54-62.
Shapiro I.D. Immunity of field crops to insects and mites. L., 1985, pp. 140-151.
Shkurpela I. Swedish fly and smut. // Protection of plants from pests and diseases, 1965, 5, p.59.
Yugenheimer R.W. Corn and its improvement. M., Kolos, 1979, 519 p.
Yurku A.I., Lazu M.N. Genetic aspects of corn smut resistance. Chisinau, 1987, p. 177.
Yakovleva N.P. Tissue and age specialization of the causative agent of bladder smut. // Bulletin of agriculture. Sciences, 1963, 2, pp. 45-51.
Agrios G. N. Transmission of plant diseases by insects. // Plant pathology (4th ed.). Academic Press, San Diego, California. Anonymous. Compendium of Diseases. 1997, b. 442-445.
Barnes C.W., Szabo L.J., May G., Groth J.V. Inbreeding levels of two Ustilago maydis populations. // Mycologia, 2004, 96, p.1236-1244.
Bojanowski J. Studies of inheritance of reaction to common smut in corn. // Theoret. and Appl. Genet., 1969, 39, 1, p. 32-42.
Boving A.G., Graighead F.C. An illustrated synopsis of the principal darval forms in the order Coleoptera. // Entomologia Americana, 1931, 1, 1, p.351.
Brefeld O. Untersuchungen aus dem Gesammtgebiete der mykologie. XI. Die Brandpilze. II Die Brandkrankheiten des Getreides. Munster, 1895, 98 s.
Christensen J., Schneider C. European corn borer in relation to shank, stalk and ear rots of corn. // Phytopathol., 1950, 40, 3, p.284-291.
Christensen J.J. Corn smut caused by Ustilago maydis. // The Amer. Phytopath. Soc. Monograph., 1963, 2. pp. 12-20.
Christensen J.J., Stakman E.G. Physiological specialization and mutation in Ustilago zeae. // Phytopathol., 1926, 16, 2, p. 979-999.
Clinton G.R. Smuts of Illinois agricultural plants. // III Agr. Exp. Sta. Bul., 1900, 57, p. 289-360.
Davis G.N. Corn latent and expressed. // Phytopath., 1936, 26, 1, p.91.
Davis G.N. Some of the factors influencing the infection and pathogenicity of Ustilago zeae(Beckm.) Unger) on Zea mays L. // Iowa Agric. Exp. Sta. Res. Bul., 1936, 199, p.247-258.
Doehlemann G., van der Linde K., Aßmann D., Schwammbach D., Hof A., et al. Pep1, a secreted effector protein of Ustilago zeae, is required for successful invasion of plant cells. // PLoS Pathog., 2009, 5(2): e1000290. doi:10.1371/journal.ppat.1000290.
Dolinka B. Otpornost i tolerantnost kukuruza prema aved-skoj masci i kukuruznom plamenae v Nartonvasaru. // Savremen.Poljopr., 1969, 17 p.
du Toit, L. J., and Pataky J. K. Effects of silk maturity and pollination on infection of silks to maize ears by U. maydis. //Plant Dis., 1999, 83, 7, p. 621-626.
Dungan G.H. Woodworth C.M. Loss resulting from pulling leaves with tassels in detasseling corn. // Agron. J., 1939, 31, p.872-875.
Garber R.J., Quisenberry K.S. Breeding corn for resistance to smut ( Ustilago zeae). // J. Amer. Soc. Agron., 1925, 17, p.132-14.
Gilbertson R.L., Manning W.J., Ferro D.F. Association of the asparagus minor stem rot caused in asparagus by Fusarium species. // Phytopath., 1985, 75, 11, p.1188-1191.
Grogan C. Detasseling responses in corn. // Agron. J., 1956, 48, 6, p.247-249.
Nanna W.F. Studies in the physiology and cytology of Ustilago zeae and Sorosporium reilianum. // Phytopath., 1929, 15, 5, 415-441.
Harris M, Frederiksen R. Concepts and methods regarding host plant resistance to arthropods and pathogens. // Ann. Rev. Phytopathol., 1984, 22, p, 247-272.
Hitchcock A.S., Norton J.B.S. Corn smut. //Kans. Agr. Exp. Sta. Bul., 1896, 62, 169-212.
Holiday R. Genetic of Ustilago maydis. // Genetic Res., 1961, 2, 2, p. 204-231.
Hooker A.L. Inheritance of mature plant resistance to rust in corn. // Phytopathol., 1967, 57, p.815.
Huttig W. Uber der temperatur auf die keimung und geschletsverteilung bei brandpilzen. // Z. Bot., 1931, 24, s.529-557.
Immer F.R. Inheritance of reaction to Ustilago zeae in maize.// Agron. and Plant Genetics, 1927, 51, p.599-602.
Immer F.R., Christensen J.J. Determination of loses due to smut interaction in selfed lines of corn. // Phytopathol., 1928, 18, p. 599-602.
Immer F.R., Christensen J.J. Further studies on the relation of corn to smut and effect of smut on yield. // Phytopathol., 1931, 21, p. 621-674.
Ivanovic M. Uticaj virusnog mozaika kukuruza na osetlivost gljivi kukuruza prema Ustilago maydis. D.C. Corda. // Zastita Bijya, 1979, 30, 148, s.135-140.
Jenkins M.T. Correlation studies with inbred and crossbred strains of maize. // J. Agr. Res., 1929, 39, p.677-721.
Jones D.F. Segregation of susceptibility to parasitism in size. //Amer. Jour. Bot., 1918, 5, p. 295-300.
Kahmann R. Establishment of compatibility in the Ustilago maydis. //Maize pathosystem. J. Plant Physiol., 2008, 165, p.29-40.
Koehler B. Corn ear rots in Illinios. //Ill. Agr. Exp. Sta. Bul., 1959, 69, 87 p.
Kyle C. Relation of husk covering to smut of corn ears. //U.S. Dept. Agr. Techn. Bul., 1929, 120, p.1-7.
Martinez-Espinoza A.D., Leon-Ramrez C.G., Ruiz-Herrera N.S.J. Use of PCR to detect infection of differentially susceptible maize cultivars using Ustilago maydis strains of variable virulence. // Published online: 24 May 2003, Springer-Verlag and SEM 2003.
Middendorf M. Untersuchungen uber methoden sur infection mit mais brend ( Ustilago zeae) und ichre aihangigheit von alter temperature und sorte. // Der Zuchter, 1958, 28, 2, s. 92-93.
Mills L.I., Kotze I.M. Scanning electron microscopy of the germination growth and infection Ustilago maudis on size. // Phytopathol. Z., 1981, 102, 1, p. 21-27.
Munteanu I., Cabulea I, Radulescu E. Studies in immunity and inheritance of corn response to Ustilago maydis(Dc.) Corda. // Savremena Poliopr., 1969, 17, 5-6, p. 407-415.
Palmer L., Kommedahl T. Root infecting Fusarium species in relation to rootworm infestations in corn. // Phytopathol., 1969, 55, 11, p.1613-1617.
Platz G.A. Some factors influencing the pathogenicity of Ustilago zeae. //Jowa State Coll. J. Sci., 1929, 3,. p.177-214.
Rowell J.B., De Vay J.E. Genetics of Ustilago zeae in relation to basic problems of its pathogenicity. // Phytopath., 1954, 44, 4, p. 356-362.
Sabbagh S.K., Martinez Y., Roux C. Root penetration of maize by Ustilago maydis. // Czech. J. Genet. Plant Breed., 2006, 42, p.79-83.
Schmitt C. G. Cultural and genetic studies on Ustilago zeae. // Phytopath., 1940, 30, 5, p. 381-390.
Scurti J. On the morbid histology of maize attaced by Ustilago maydis.// In: Annali Della sperimentazione agragia, niova serie, 1950, 4, 5, p. 827-855.
Stakman E.C., Tyler L.J., Hastad.G.E. et al. Experiments on physiologic specialization and nature of variationig Ustilago zeae.// Phytopath., 1935, 25.
Stakman E.G., Christensen J.J. Problems of variability in fungi. In: Plant Diseases. The Yearbook of Agriculture. U.S. Dept. of Agriculture, 1953, p.35-62.
Tu L., Ford R. Maize dwarf mosaic virus predisposes corn to rot root infection. // Phytopath., 1971, 61, 7, p.800-803.
Vǒzdova G.M. Metodiké otazky hodnoceni kukurice na odolnost ke sneti kukuřice ( Ustilago zeae(Beckm.) Unger). // Sbornik ved. praci Vuku, 1965, 1, s. 55-73.
Walter J.M. Factors affecting the development of corn smut Ustilago zeae(Beckm.) Unger. //Minnesota Agric. Exp. Sta. Techn.Bul, 1935, 111, 65 p.
Walter J.M. The mode of entrance of Ustilago zeae into corn plants. // Phytopathol., 1934, 24, p.1012-1020.
Wheeler Q., Blackwell M. Fungus - insect relatioships. 1984, 514 p.
Zambino P., Groth J.V., Lukens L., Garton J.R. May G. Variation at the b mating-type locus of Ustilago maydis. Phytopath., 1997, 87, pp. 1233-1239.
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