Blasticidin S (BcS) and puromycin (PM), inhibitors against protein synthesis in fungi and higher organisms, inhibited tobacco mosaic virus (TMV) multiplication in tobacco leaf-discs, whereas chloramphenicol (CM), inhibitor against bacterial protein synthesis, did not inhibit. TMV produced by antibiotics treatment had the same infectivity as that produced by untreatment. BcS and PM inhibited 14C-leucine incorporation into the cytoplasmic protein of tobacco leaf-discs, but CM did not. CM reduced more rapidly the chlorophyll content in leaf-discs than BcS and PM. 14CO2-incorporation into infected leaf-discs was strongly inhibited by CM, but not by BcS and PM. Although, under BcS and PM treatments, the rate of 14C-amino acids and 14CO2-incorporations into TMV was in proportion to the amount of TMV produced, the rate of the former incorporation rather increased by CM under both light and dark conditions and that of 14CO2-incorporation was decreased, whereas the amount of TMV was not altered by CM. Most of 14CO2 incorporated into TMV located in TMV protein. Site of TMV synthesis in tobacco leaf-discs and the role of photosynthetic activity of chloroplasts are discussed.
Metabolism of pentachloronitrobenzene (PCNB) by phytopathogenic fungi was studied with reference to selective toxicity. PCNB is metabolized to two substances, pentachloroaniline (PCA) and pentachlorothioanisole (PCTA), by Fusarium oxysporum f. lycopersici. Antifungal activities of PCA and PCTA against phytopathogenic fungi are extremely inferior to that of parent compound, PCNB, which indicate that these two biotransformation reactions belong to detoxication. Metabolism of PCNB to PCA is common to various microorganisms, but metabolism of PCNB to PCTA is specific for some filamentous fungi. Judging from these findings, it is impossible to elucidate selective action of PCNB from only presence or lack of PCNB degrading ability of microorganisms.