Fascist Pigs: Technoscientific Organisms and the History of Fascism

But scientific triumphs are never easy. By 1932 the von Kameke seed company of Streckenthin (Brandenburg) had reported that the W-varieties it was working with had undergone a severe attack of late blight.[91] According to R. Steven Turner, this event marked the beginning of the fall of the heroic age of late blight resistance breeding. Rudolf Schick of the Kaiser Wilhelm Institut für Züchtungsforschung, was quick in criticizing Müller for not having anticipated such possibility. Schick was referring in concrete to the existence of different biotypes of the fungus, which explained the vulnerability of the W-varieties. Contrary to initial hopes, Phytophthora infestans was able to develop new biotypes, a problem plant breeders were very well aware of from their previous experience with the black stem rust of cereals. By 1936, scientists at the Kaiser Wilhelm Institut für Züchtungsforschung had identified eight different biotypes of P. infestans.[92]

By 1935, Müller was already acknowledging in the pages of Der Züchter (The Breeder), the main journal of German academic breeders, that “the W-varieties do not constitute a permanent solution” to late blight.[93] Nevertheless, Müller was confident enough to conclude that same article with a grandiloquent statement boasting about his knowledge of the enemy and “the methods with which to wrestle him to the ground.” And apparently the work with the W-varieties had earned Müller enough of a reputation to convince the leadership of the BRA to establish, in 1936, a new branch in Eichhof (Pomerania) dependent of his own Genetics and Breeding Section of the Botany Department. In September 1935, in his plea to the BRA’s director that 110,000 Reichsmarks be spent at the new branch for the acquisition of experimental fields and the building of greenhouses and laboratories, Müller explicitly linked the identification of new strains of Phytophthora infestans with increasing demands on the breeding work.[94] Different pathogen strains implied the multiplication of the inoculation work, which justified the testing of about 12,000 potatoes to begin with. The additional difficulties didn’t sway him from suggesting to the BRA’s director that sooner or later the best W-varieties produced by the BRA’s new department would make their way to the German fields.[95] Confirming Müller’s promises, in 1940 three new Phytophthora-resistant commercial varieties—named Erika, Robusta, and Frühnudel—were added to the Reichssortenlist, followed by Aquila in 1942.[96] The fungus was not to play the same decisive role in World War II that it had played in the previous conflict.[97]

What may have constituted a serious blow to Müller’s research was thus turned into a justification for more resources: more strains of the fungus demanded more testing of breeding lines, leading to new greenhouses, laboratories, and experimental plots. More than that, it led Müller and his team at the BRA to delve deeper into the mechanisms of resistance reactions in potatoes.[98] What hindered the development of Phytophtora infection was first explored by Müller in 1931, when he scrutinized potato specimens through cytological-physiological methods, reaching the conclusion that infected potatoes released some kind of toxic substance to the fungus.[99] Having previously established the existence of a dominant Mendelian factor (the R-gene) responsible for the resistance of the W-varieties, Müller was now interested in its mode of action. Close observation of infected materials of different varieties suggested that the alleles present in the W-varieties induced a predisposition for the host tissues to “acquire” a local immunity from infection when in contact with the hyphae of P. infestans. Comparison of susceptible and resistant potato varieties revealed that in both varieties host cells were destroyed after contacting the protoplasm of the parasite. If morphological and physiological analyses revealed the same final effect, the difference in degree of resistance depended on the rapidity of the reaction. Further penetration of the hyphae was made impossible by the rapid reaction of the host tissue. In other words, Müller established a relation between the degree of resistance and the velocity of the “defense necrosis” reaction of the host tissue. The R-gene controlled the speed of the reaction without changing its basic nature. Much of the work of Müller’s team at the BRA during the Nazi years dealt directly with the exploration of such mechanism.[100]