1957 Volume 22 Issue 2 Pages 75-78
In the author's former report 5-8, it was shown that the content of epidermal midrib cell of resistant potato varieties degenerates according to the following scheme, when infected by P. infestans. To ascertain whether such a chain of cell physiological phenomena in degeneration process is in a causative linkage or not, following experiments were carried out. Petioles of Hokkai No. 10 (inter-specific hybrid variety) were cut in halves longitudinally, and washed with running water, and then the cut surfaces were inoculated with zoospore suspension of P. infestans (race O). The variety used is highly resistant to race O. About 2.5hrs. after inoculation, 2, 4-dinitrophenol (DNP) 5×10-4M. solution or H2O (as control) was vacuum-infiltrated into the inoculated tissue, which was left in the solution for 30min. Then the tissues were kept in petri dishes at 19-20°C. DNP is known to be an inhibitor of oxidative phosphorylation, and poisonons for protoplasmic streaming. At the time when the tissues were vacuum-infiltrated, a large number of appressoria were beginning to extend the infection hyphae into the host cell. The vitality of the infected cells was judged by means of vital staining with neutral red or by recognizing the existence of protoplasmic streaming. The results obtained are graphed in fig. 1. The death of the invaded cell was remarkably delayed by the post-infectional DNP treatment. Accordingly it will be presumed that acceleration of cytoplasmic movements induced by infection of P. infestans is closely associated with the death of that invaded cell. In addition, it will be reasonable to suppose that the energy is required for the quick occurrence of the death of the hyper-sensitive cell invaded by P. infestans. Other possible explanations of the delay of the cell-death by post-infectional DNP treatment, however, should not be overlooked. It is possible that the effect of DNP upon the intra-cellular hyphae gives rise to the delay of the cell-death. In fact, the velocity of development of intra-cellular hyphae in a cell treated with DNP was inhibited by about 30% as compared with that in untreated one (Table 1). The vigorous hyphal growth in later stages in the living cells treated with DNP, however, seems to indicate that the effect of DNP upon the hyphal development cannot be the cause of delay of the cell-death. It is possible, however, that the treatment would affect the production of toxic substance by intra-cellular hyphae of P. infestans, had it been really produced, thus inducing the delay of cell-death. This possibility should be ascertained in future expemiments.
