<abstract language="eng">The present paper gives some observations on the tumour formation and other abnormalities observed in the interspecific hybrids, Nicotiana glauca x N. Langsdorffii and N. glauca x N. Sanderae. Without entering into a detailed discussion of the literature and the various speculations proposed by Kostoff and Whitaker about the causes of tumour formations or on the relations between "spontaneous" and pathogenic tumours (Kostoff, Levine and others), two new observations are described. 1) The abnormalities in the two above mentioned hybrids are quite different. As already reported by other authors, the hybrids N. glauca x N. Langsdorffii are initially quite normal and vigorous, while tumours and other proliferations, on the stem, the stem base and the root appear more or less frequently in older plants. Tumours on leaf are rare and flowers are normal (fig. 1,2,7 and 10). The hybrids N. glauca x N. Sanderae are very different from the former. These remain either weak and rachitic, forming early large tumours at the stem base and on the root (fig. 5 and 6 right half). Numerous shoots with more or less normal leaves may arise from these tumours (fig. 11 and 12). Or the plants show an extremely vigorous and abnormal ramification with a number of serial axial shoots developing in each leaf axis (fig. 3 and 4). The leaves are frequently deformed and the flowers exhibit abnormally coloured patches. When crossing N. glauca with F1 (N. Langsdorffii x N. Sanderae) the offspring could clearly be divided into two groups : plants exactly as described for N. glauca x N. Langsdorffii and others which correspond to the types of N. glauca x N. Sanderae. Thus it seems that we are dealing with a monogenic differences, each species, N. Langsdorffii and N. Sanderae, being homozygous for one allele each. These alleles have no phenotypic effect in either pure species, but only in hybrids when combined with the genom of N. glauca. The situation is somewhat similar to the sublethal genes reported in interspecific crosses involving N, longiflora (Brieger, 3) and Crepis tectorum (Hollingshead, 8). Since the hybrids with N. glauca are completely sterile, it cannot be decided whether the genes reported are only modifiers or are actually causing the tumour formation and the other abnormalities. 2) A histological study was made about the origin of stem tumours. The first sign is the activation of cells of the tissues between epidermies and collenchyma. Some cells adjoining other which are dead or dying start to grow and later on to divide, in the manner typical for cells under the action of traumatic hormons (cf. Brieger, 2). Later on the whole region is activated and the cortex layers degenerate. At this stage large tumours may be formed, but as yet without connection with the xylem (fig. 15). Later on the cambium and the secundary medulary rays participate in the irregular development (fig. 13) which finally reaches the medulla. Finally the central cylindre is forced open and the tumours connected with it (fig. 14). Thus tumours formation on the stem is endogeneous and starts from mature cells, not from meristematic cells. 3) Finally an observation is reported, without an attempt to explain it. In the earliest phases of tumours formation in the stem and in cells not participating it, intracellular bodies are observed (fig. 17) with a colourless membrane and on alveolar and highly refractive content. These bodies resemble somewhat cells of fungus such as Chytridiales, but, as already said, their nature is obscure
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