Auxin-Kinetin Interaction in Tissue Cultures of Nicotiana Species & Tumor-Conditioned Hybrids.

Historically, nmuch of the research in plant tumor physiology and growth has utilized cultures derived from bacterial infection and wounding. Observation of these systems has demonstrated that the transformation of a nornmal cell to a tumor cell in the crown-gall disease involves progressive activation of certain biosynthetic systems. According to Braun and Wood (3) transformed cells become autonomous for auxins and kinins as well as for other compounds. On the other hand, it has been reported that tumor cells of Picea glauca have an absolute auxin requirement for growth (6). In earlier work with Nicotiana species and hybrids on the conversion of tryptophan to auxin it was suggested that high auxin levels might contribute to undifferentiated growth in the tobacco hybrid system (8). Thus, the Nicotiana parental species, which do not forml tumors, and their tumor forming hybrids and amphiploids seem to offer excellent experimental nmaterial to explore and further clarify the suggested differences in the hormonal requirements of tumor and nontumor forming tissues. If an imbalance in the auxin system is in fact responsible for tumor induction in vivo, it should be possible to demonstrate a differential hormone requirement for the tissue cultures of nontumorous parental species and their tumor forming hybrids. One purpose of this study was to (letermine the tissue culture requirements of tumor and nontumor forming tissues of Nicotiana. Another purpose was to test specifically with the tobacco hybri(d systenm Braun's findings (1, 2) regarding fundanmental changes accompanying the conversion of normal cells to tumor cells by crown-gall bacteria. The data presented show not onl) a marked difference in the auxini requirement of tumorous vs. nontumorous tissue but indicate that exogenous kinetin is an important and consistent requirement for growth of tissues of the nontumor forming types. There is also a synergistic effect of auxin and kinetin.