Investigations in 1937 by F. G. Larmer, of the Department of Agriculture, on the phoma root rot of sugar beets gave some interesting results. Phoma betae, the causal organism, occurs rather generally in sugar beet tissue. The fungus is apparently seed-borne, and young plants may be killed by severe attack. Under ordinary conditions it appears to live in the beet plant without provoking any visible symptoms. If the sugar beet lags in its growth because of drought or lack of soil nutrients, the fungus may produce extensive and conspicuous decay of tissue. In the fall the fungus causes serious rotting of sugar beets in storage piles. Larmer found that well-nourished sugar beets, grown with adequate water supply, kept better in storage than sugar beets from the check plots that suffered from drought and poor soil conditions. The effects of plant food elements, especially phosphorus, were decisive. Sugar beets, grown with adequate phosphate, showed minimal decay as compared with serious decay in the sugar beets not receiving additional phosphorus. Inoculation tests were made with Phoma betae and showed that the plants grown with adequate phosphate definitely resisted invasion by the fungus, whereas the sugar beet roots grown with limited phosphate decayed. The practical applications of the experiments are obvious and afford an accessory advantage, besides crop increase, to be derived from appropriate applications of fertilizer. But the point to be stressed is that it seems definitely to be shown that plants whose nutrition was adequate, especially with respect to phosphate, were more resistant to Phoma betae. In recent experiments, adequate nitrogen nutrition has given improved keeping quality to sugar beets.

Black root of sugar beet has been found to be a disease complex, consisting of an acute form caused by the ordinary damping-off organisms and a chronic form caused by Aphanomyces cochlioides. Black root is most serious on soils of low available phosphate. Poor stands that result from attack of the soil organisms may be prevented by proper phosphate fertilization. A plausible explanation of the better stands that accompany liberal applications of P₂ O ₅ fertilizer is that phosphate makes the young sugar beet plants more resistant to the pathogens. The effect must be upon the beet, because abundant trial has failed to indicate any effects upon the fungi from comparable phosphate feeding. Black root control now is based on two things: First, the production of varieties that combine resistance to black root and to leaf spot; second, proper fertilization of the resistant variety with P₂O₅ and other necessary food elements. A favorable environment for the sugar beet increases the advantages that come from disease resistance.

The associative effects of nutrition and disease are not unique in phytopathology. Pronounced fungus invasion occurs with certain deficiency diseases; for example, the fungus rots or severe outbreaks of mildew that occur on plants short of boron. Existence of fungus disease does not of itself indicate malnutrition, but the association of disease and poor plant feeding is frequent. Sugar beet plants growing with scant phosphate show severe leaf injury following spotting of the leaves by Cercospora beticola, not because the leaf spot fungus is more aggressive but because weak parasites such as Alternaria can now invade and greatly en-large the cercospora spots. The secondary attacks following leaf spot of this type do not occur with well-nourished plants. With many important plant diseases, the host-parasite relationships are very delicately balanced, and proper feeding of the crop plant may be highly important.

The nature of disease causation and of plant response may at first glance seem to contribute little to the practical problems of disease-resistance breeding. These seem to be moving along, with little reference to the theory. It is not unusual for practical applications to go far beyond the scientific explanation of phenomena just as a driver may run a machine without understanding the mechanism or the source of power. But always in science the theoretical basis is the fruitful source of new concepts and new approaches.

We are concerned with the ways and means of the pathogen's attack and of the host plant's defense. With hundreds of thousands of pathogens, each composed of numerous biotypes, we cannot expect a single pattern of disease production or to find some specific substance that confers resistance. Thus, the theory is important in teaching what not to search for. The theory is important also in its teachings with regard to plant reactions. As I have brought out, disease exposure must be maximum, and knowledge of plant pathology must be put into service to initiate infection, produce disease, and finally to classify affected plants. The theory teaches also the specificity and delicateness of the interactions that exist between host and parasite, and the play of environmental factors as they influence these reactions. Thus light, temperature, length of day, nutrition, and the entire range of physiological forces are concerned. Plant response when subject to the parasite is the sum total of these effects. The goal of breeding for disease resistance is to manipulate host and parasite and the factors playing upon them in such a way that for a given environment disease-safe varieties may be provided.

The fungi, bacteria, and the viruses, each in its own specific manner, establish a food and water relation with the host plant. The invader may be tolerated; it may dwarf the plant or cause overgrowths or decay; it may kill the host. The tools the invader uses are enzymes and toxic substances; in considerable part, mere occupancy of the cells, appropriation of food, and the effects of the metabolic byproducts from the growth of the pathogen may be sufficient to explain the disease signs and symptoms.

Disease resistance as considered here is that which is of protoplasmic origin, as opposed to mechanical walling-off, escape, or other reactions than purely vital ones. We do not know at all what makes one plant less susceptible than another, nor do we know the basis of fungus specificity that makes one species, genus, or family of plants completely immune from a given parasite. Of the two hypotheses commonly advanced, antagonism (presumably chemical) and the so-called starvation hypothesis, the latter seems most tenable, with nitrogen nutrition appearing to be a significant phase.

Despite the common question posed by farmers, we do not know how to feed plants so as to make them more disease-resistant. Until recently, research along this line has been neglected. There are also strong indications that disease-resistant varieties may be made to do better by proper nutrition. The next decade may see important developments as the nutrition of our crop plants is studied from the point of view of plant disease control.

GEORGE H. COONS was loaned in 1924 and in 1925 to the Bureau of Plant Industry, Soils, and Agricultural Engineering by the Michigan State College, where he was professor of botany, to initiate the research program of breeding varieties of sugar beet resistant to curly top and to leaf spot. After his return to the College, he continued as plant pathologist on a half-time basis with the Bureau until 1929, when he left Michigan State College to become principal pathologist in charge of sugar beet research projects in the division of sugar plant investigations. He received his undergraduate training at the University of Illinois, his master's training at the University of Nebraska, and his doctorate at the University of Michigan. After directing the sugar beet project of the Bureau for 23 years, he left administrative work to conduct research, particularly on virus yellows.