Abstract
The purpose of this research was to determine how the pathological effects characteristic of wilt of the tomato (Lycopersicon esculentum) are produced. This disease, which is caused by the filamentous fungus, Fulsarium lycopersici, is characterized by gradual or sudden loss of turgor in the leaves and stems, and generally by eventual dessication and death. Internally, the most characteristic symptom is a decided vascular discoloration (necrosis). Precedent to, or accompanying loss of turgor, local or general chlorosis of the leaves often occurs. In fact, at times, when environmental factors, particularly temperature, are not optimal for the pathogen chlorosis, and resultant retarded or arrested growth of the plant are the outstanding or only external symptoms, so that the disease resembles a show blight.
The pathogen lives primarily in the xylem elements of the host. Following the early work of Smith, 1 who established that wilting in bacterial wilt of cucurbits is essentially due to a clogging of the vessels, it has been assumed quite generally that in such vascular mycoses as tomato wilt and cabbage yellows, the parasite affects the host by clogging the water conducting elements and thus mechanically interfering with the water supply of the transpiring top of the plant. A considerable body of observational and experimental data, especially by Clayton, 2 suggests that this hypothesis alone is not adequate. A different, or an additional possibility is that the fungus produces or induces the production of substances which exert a slow and progressive, or a sudden and rapid toxic effect on the cells of the host.
In these experiments we were especially concerned in testing the validity of the second hyphothesis. Pure cultures of the fungus were grown for various lengths of time in various volumes of a synthetic medium which consisted of 1,500 cc. of H2O, 50 grams of C12H12O11, 10 grams of KNO, 5 grams of KH2PO4, 2.5 grams of MgSO4, and a trace of Fe2Cl3.
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