Tobacco plants carrying a tms locus of Ti-plasmid origin and the Hl-1 allele are tumor prone.

The autonomous growth of plant tumor cells is believed to result from their persistent loss of the requirement for growth hormones such as auxin and cytokinin. The partially dominant gene Habituated leaf-1 (Hl-1) regulates the requirement of cultures tissues of Havana 425 tobacco (Nicotiana tabacum L.) for cytokinins. The Hl-1 allele can partially restore the tumor phenotype in tobacco cells transformed with a Agrobacterium tumefaciens Ti plasmid defective in the isopentenyl transferase locus, which encodes a key enzyme in cytokinin biosynthesis and is required for neoplastic growth. To investigate the oncogenic function of Hl-1, we transformed wild-type (hl-1/hl-1) and Hl-1/Hl-1 tobacco plants with the tms locus derived from the limited-host-range Ti plasmid pTiAg162. This locus encodes enzymes for biosynthesis of the auxin indole-3-acetic acid. Grafting tests and measurements of the hormone requirement of cultured explants show that wound-induced overgrowths arising in tms transformed Hl-1 plants are tumorous. While some wound-induced overgrowths also formed in hl-1/hl-1 transformants, these showed slight hormone-autotrophic growth and weak tumorigenicity in grafting tests. In addition, Hl-1/Hl-1 tms/tms plants, but not hl-1/hl-1 tms/tms plants, spontaneously developed rooty teratomatous overgrowths, showed flowering abnormalities, and formed calli at the base of the stem in young seedlings. Thus, Hl-1 tms plants exhibit a tumor-prone phenotype, and in this regard closely resemble tumor-prone hybrids that arise in certain interspecific crosses of Nicotiana species. Our results show that the interaction of just two genetic elements-the mutant Hl-1 allele of the tobacco host with tms genes of Ti plasmid origin-are sufficient for a tumor-prone phenotype.