It was found that a 0.3mcg/ml water solution of streptomycin at first inhibits the growth and later causes the death of Ps. solanacearum, while a concentration of 1mcg/ml is required to inhibit the growth of Ps. tabaci which can be sometimes resumed later. Both bacteria were killed at once by 5mcg/ml solution.
And the writers have studied surface absorption of streptomycin in tobacco plants from various points of view, namely absorption in various plant organs, absorption amount and concentration, absorption and surface active agents, absorption and light, absorption rate and streptomycin injury to the plant.
It was found that amount of streptomycin absorbed by the lower surface of a leaf is twice as large as that absorbed by the upper surface. The higher the concentration the larger amount of streptomycin is absorbed but from a certain limit upwards the injury inflicted upon the plant increases. By adding as a surface active agent 0.1% Tween 20 the absorption was improved and the difference between the lower and the upper leaf surface became smaller. The maximum of absorption was reached 8 hours after spraying. There was no correlation between light and absorption. The plants could recover when the injury was not severe.

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The results of experiments on the epidemiology and control of Chrysanthemum white rust caused by Puccinia Horiana P. Henn. are given in this paper.
1. Teleutospores germinate at wide range of temperature from 6°C to 36°C, and optimum lies between 18°C and 28°C. Sporidia are formed at the temperature range between 6°C and 24°C, and optimum lies between 13°C and 22°C. On the affected leaves, sporidial formation is observed 6 hours after incubation at 24°C in the dark, but is inhibited by the light.
2. Sporidia germinate at wide range of temperature from 6°C to 36°C and optimum lies between some 13°C and 18°C. The light showed no effect on the germination of sporidia.
3. According to the results of the inoculation experiments, incubation period of the disease is about ten days long.
4. Teleutospores on sorus lost their vitality after 20 days in the laboratory condition in May, but at 32% of relative humidity they survive for 30 days long.
5. Sodium pentachlorophenate (PCP-Na), wettable sulfur (Soid) and flower of sulfur showed remarkable effect in retarding the germination of teleutospores on the leaves, but ammonia bordeaux, copper-mercury fungicide, mercury fungicide and lime sulfur showed little effect in retarding the germination of spores.
6. Wettable sulfur (Soid) showed the most remarkable effect in retarding germination of sporidia, and flower of sulfur and Ceresan-lime dust were the next. And yet Phygon, SR-406 and lime sulfur showed also considerable fungitoxicity.
7. Dusting of wettable sulfur seems to be effective in controlling the present disease.

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A new disease of carrots showing a stunted, unthrifty appearance suggestive of mineral deficiency has been noted in Kanto District since 1951. Foliage symptoms consisted of irregular chlorotic mottle, yellow veinclearing, and distortion or reduction in size of leaflets. Sometimes growth stunting and rosette were severe. No necrosis was observed on leaflets, stems and roots.
The disease was proved to be caused by a virus, which is transmitted by the aphid Brachycolus heraclei, a common infestant on carrot in Japan, but not by Myzus persicae. Negative results were obtained by mechanical inoculation with carborundum or pin-puncture method, and there was no evidence of transmission through carrot seed.
The vector acquired the virus after an infection feeding period of 1 to 24 hours and viruliferous aphids could transmit with an inoculation feeding for 24 hours. The virus was of a persistent type and viruliferous vector remained infective for a period of up to fifteen days in a series of transfer experiments. There appeared to be no evidence of the presence of a latent period in its vector.
Carrot was the only known natural host of the virus. Celery was experimentally infected, but Cryptotaenia canadensis and parsley were not infected.
From the symptoms, the mode of transmission, restricted host range, long persistence in its vector etc., the virus, in consideration, may be closely related with the carrot motley dwarf virus described by Stubbs (1948) in Australia.
With cucumber mosaic virus from petunia, mechanical inoculation to carrot failed to produce infection.

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1) In the present paper, the authors deal with the results of the experiments on the identification and isolation of wilt toxin by Fusarium bulbigenum var. niveum causing watermelon wilt.
2) It was recognized that the wilt toxin, metabolited in the cultured filtrate was thermostable, non-volatile, dialyzable and adsorpted by 2% active carbon under a alkaline condition.
3) Parallel was probably established between resistance and susceptibility of watermelon varieties to Fusarium wilt and sensitivity to cultured filtrate injury.
4) Isolation processes of wilt toxin involved in the cultured filtrate or its mycelial mats were summarized as follows: The filtrate adjusted at pH 8.5 was adsorpted by 2% active carbon, its adsorpted carbon or dried mycelial mats were then eluted by aceton. Aceton solution was concentrated and dried up under a diminished pressure, resulted rich water residue was adjusted by NaHCO₃ at pH 8.5, and then effective principle was extracted with ether. When ether solution was slowly concentrated, effective principle substance was precipitated. By recrystallizing from aceton, wilt toxin was obtained as crystal. The substance was prism like crystal, m. p. 138∼9°C., and soluble in alcohols, aceton, ether, chloroform, carbon tetrachloride or benzene, and insoluble in water, acid, alkali or ligroin.
5) The present wilt toxin isolated was designated by the authors phytonivein. Watermelon cut stems and seedlings were permanently wilted by 10^-5 phytonivein solution.

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In the present study a series of experiments were carried out to measure the time required for young midrib cell of resistant and susceptible potato varieties to become brown when infected with Phytophthora infestans. The varieties used in the experiments are 41089-8 (Solanum demissum×S. tuberosum) as the resistant one, and Hokkai No. 9 (S. tuberosum) as the susceptible one. As has been shown in the former reports^{9, 10)} when microscopical observation is successively made on the same living section, the degeneration process seems to be retarded by the injury caused in the act of handling.
Accordingly in the present study microscopical observations were made always on fresh and living sections stripped by razor at a definite interval of time 10-20min. (in the case of 41089-8) or 1-several hours (in the case of Hokkai No. 9) after inoculation. The observations were finished in short time. Inoculation experiments were repeated 14 times in the case of 41089-8, and 7 times in the case of Hokkai No. 9.
Seven phases were distinguished in the process of infection of the host cells by P. infestans. The number of cells belonging to each phase was divided by total number of cells observed and expressed in percentage in figs. 1 and 2. By plotting the values thus obtained as ordinates against time as abscissas, the curves shown in figs. 1 and 2 were obtained. From these curves, the time required for completion of each phase of the degeneration process of cells infected by P. infestans may be deduced (Table 1).
About 12/3∼2 hrs. after inoculation, penetration was observed on midrib epidermis of the resistant variety, showing no difference from that in the susceptible variety. After the fungus penetrated into the cell and formed the primary intra-cellular mycelium, remarkable differences in the degeneration process of cells began to be observed between the two varieties.
In the midrib cells of the highly resistant variety“41089-8”, within 10min. to 1 hour after completion of penetration, the first sign of injury appeared; the granules in Brownian motion appeared around the infected loci. About 10 minutes to 1 hour after the appearance of such granules, the contents in the infected cell began to discolor. Within about 10 minutes to 30 minutes after the beginning of discoloration, the granules stop their movement, and the cell content seems to gelatinize. In midrib cells of the susceptible variety, on the contrary, the granules in Brownian motion do not appear in the infected cell until 2 to 8 hours after the completion of penetration. Within about 7 to 10 hours after the appearance of such granules, discoloration of the content in infected cell does not take place. The granules stopped their movement 1 to 11/2 hours after discoloration of cell contents.
In such process of reaction of the resistant and susceptible varieties, the most quick degeneration was observed in the basal tissue of midrib of unfording leaflets. The time required for degeneration seems to be greater in the tissues of comparatively older leaflets than in younger ones.
Within about 10 hours after gelatinization of cell contents in infected cells, the brown color of that cell becomes deeper and finally blackish brown. Thereafter, however, it seems that further deepening in color in infected cells does not take place. Such deepening in color suggests that the deposition of polyphenol and other compounds in the browned infected cell continues for a comparatively longer period after the collapse of that cell.

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