92 Journal of Agricultural Research 



Vol. V, No. 3 



fields not sprayed with Bordeaux mixture; in other words, epidemics 

 were started from the small areas found early in the season. The 

 spread of the disease was wholly comparable to the above-described 

 developments on the small plot at Madison. 



Last summer (191 4) three similar infection centers were found in 

 fields near Presque Isle, Me. Such a center is shown in Plate VIII, figure 2. 

 The infected area is set off by a white line. The question naturally 

 arises as to how these centers come into existence. Are they due to 

 the planting of infected seed potatoes or to wind-blown spores? It is 

 impossible to answer either of these queries positively, but in the light 

 of evidence now at hand both are probable. There can be no doubt 

 that seed potatoes infected with P. injestans are planted by the growers. 

 This has been observed many times, and in one case 46 seed pieces in- 

 fected with late-blight were taken from a single barrel of seed potatoes 

 which were about to be planted. None of these were badly infected, 

 but such specimens are more certain to produce infected progeny than 

 those badly diseased, as the latter often rot in the ground. 



It may well be, therefore, that these infected centers originate from 

 the infected seed, even although the originally infected shoot is not 

 found. This is probably due to its rapid death after the mycelium 

 reaches the surface of the soil. It soon dries up and leaves little evidence 

 of its presence behind. On the other hand, it is easy to understand how 

 these infected centers might be caused by wind-blown conidia, but it is 

 more difficult to explain their origin without making use of the progeny 

 of infected seed tubers. Although it is not definitely shown how these 

 infected centers originate, in the case of the experimental plots it was 

 clear that they came into existence at the same time that the infected 

 shoots developed. It is also knowi. that seed potatoes infected with 

 P. injestans are planted. 



RELATION OF THE MYCELIUM IN THE SEED TUBER TO THE PROGENY 



Logical as it seems that the shoots and plants produced by diseased 

 tubers should become infected in the same way as the young sprouts, 

 such has not been found to be the case by a large majority of the students 

 of this problem. That the mycelium in the diseased tuber may renew 

 infection from one year to another was first supported by experimental 

 evidence in 1861 by De Bary (i). His evidence, however, was not gen- 

 erally accepted, and in 1876 Pringsheim (29) advanced the alternate- 

 host theory. It should be recalled in this connection that De Bary 

 announced the fundamental rediscovery of heteroecism in Puccinia 

 graminis in 1865, which probably influenced Pringsheim (29) and many 

 others in accepting the alternate-host theory as a possibility in Phytoph- 

 ihora injestans, where oospores were unknown and infected tubers 

 failed to produce infected plants. 



