Meyer A D, Aebi R, Meins F
Friedrich Miescher-Institute, Basel, Switzerland.
Differentiation. 1997 May;61(4):213-21. doi: 10.1046/j.1432-0436.1997.6140213.x.
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.
植物肿瘤细胞的自主生长被认为是由于它们持续丧失了对生长素和细胞分裂素等生长激素的需求。部分显性基因“习惯化叶片 -1”（Hl-1）调节哈瓦那425烟草（Nicotiana tabacum L.）培养组织对细胞分裂素的需求。Hl-1等位基因可以部分恢复用在异戊烯基转移酶位点有缺陷的根癌农杆菌Ti质粒转化的烟草细胞中的肿瘤表型，该位点编码细胞分裂素生物合成中的一种关键酶，是肿瘤生长所必需的。为了研究Hl-1的致癌功能，我们用源自有限宿主范围Ti质粒pTiAg162的tms位点转化野生型（hl-1/hl-1）和Hl-1/Hl-1烟草植株。该位点编码生长素吲哚 -3-乙酸生物合成的酶。嫁接试验和培养外植体激素需求的测量表明，在tms转化的Hl-1植株中出现的伤口诱导过度生长是肿瘤性的。虽然在hl-1/hl-1转化体中也形成了一些伤口诱导过度生长，但在嫁接试验中这些表现出轻微的激素自养生长和弱致瘤性。此外，Hl-1/Hl-1 tms/tms植株，而不是hl-1/hl-1 tms/tms植株，自发地形成了多根的畸胎瘤样过度生长，表现出开花异常，并在幼苗茎基部形成愈伤组织。因此，Hl-1 tms植株表现出易患肿瘤的表型，在这方面与烟草属某些种间杂交中出现的易患肿瘤的杂种非常相似。我们的结果表明，仅两个遗传元件——烟草宿主的突变Hl-1等位基因与Ti质粒来源的tms基因——的相互作用就足以产生易患肿瘤的表型。
