Walker—Nature of Disease Resistance in Plants. 233: 
protoplasm of the cells of the host to form anti-bodies which destroy such 
enzymes or toxins, or to excrete chemotactic substances which repel or at¬ 
tract the fungus-protoplasm. 
Other work on the relation of rust fungi to their hosts has been 
carried on by Gibson (36) with Puccinia (TJredo) chrysanthemi 
Roze. on chrysanthemum, Marryat (52) with Puccinia glumarum 
on wheat, by Stakman (71, 72) with Puccinia graminis on wheat, 
by Reed and Crabill (65) with Gymnosporangium juniperi-virgin- 
ianae Schw. on apple. In all cases the parasites were found to 
enter normally the substomatal chambers of both susceptible and 
highly resistant varieties of their respective hosts, but the differ¬ 
ence in resistance lay in the reaction between the fungus hyphae 
and the mesophyll cells about the substomatal chamber. Giddings 
(37) describes a gradual development of resistance to rust (Gym¬ 
nosporangium juniperi-virginianae) in the leaves of York Imperial, 
a susceptible variety of apple. He believes that this acquired im¬ 
munity is due primarily to food factors and secondarily to dif¬ 
ferences in the composition of the cell wall. 
The recent contribution by Miss Allen (2) advances considerably 
our knowledge of the nature of rust resistance. She has made 
a careful eytological study of infection of Baart, a very susceptible 
variety of wheat, and Kanred, a highly resistant variety, to a certain 
biological strain of Puccinia graminis tritici. We quote from her 
summary as follows: 
The germination of the spores and the formation of the appressoria on 
the stomata take place in the same way in the susceptible and immune hosts. 
In Baart the fungus enters freely and grows rapidly. In Kanred, under 
greenhouse conditions, only a few of the fungi pass through the stomata; 
the rest remain outside until they shrivel and die. 
In a congenial host, numerous haustoria are formed. A slender-growing 
hypha strikes a host cell, swells at the tip, its pair of nuclei divide, and 
a septum is formed, marking off a short terminal cell. This haustorium 
mother cell is closely appressed to the host cell, forms a fine pore through 
its wall and the host wall, and its contents, including both the nuclei, 
which have decreased in size, and the cytoplasm, now pass in, forming the 
haustorium. The osmotic membrane of the host appears to be invaginated 
by the haustorium, but apparently is still intact. 
In Kanred the process is similar until a small haustorium is formed, 
which, either by its presence, or, as is more likely, by secreting some 
substance in the host cell, sets up chemical reactions within that cell, 
causing its collapse and death. The further diffusion of toxic substances 
into healthy host tissues is cheeked by the formation of thickened contact 
walls. One or more of the substances formed in the host cell diffuse into 
