T-DNA of Agrobacterium tumefaciens: 25 years and counting.
T-DNA of Agrobacterium tumefaciens: 25 years and counting.
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根癌农杆菌的 T-DNA：25 年且仍在继续。
DOI：
10.1016/s1360-1385(02)02265-3
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Binns,AndrewN
中科院分区：
文献类型：
--
作者：
Binns,AndrewN
Andrew N. Binns transposon or plasmid, could carry the information specifying virulence, and, hopefully, the TIP. A second crucial observation was made by Robert Hamilton [9] who discovered that the virulent C58 strain of A. tumefacienscould be cured of its capacity to induce tumors by continuous growth at an elevated temperature (35 C). This, again, was consistent with the thought that a plasmid might encode the TIP because it was already known that many plasmids could be lost during growth at elevated temperatures. In 1974, Zaenen et al.[10] used alkaline or neutral lysis followed by sucrose gradient centrifugation and electron microscopy to provide the first evidence of a large plasmid in Agrobacterium. Moreover, they showed that avirulent strains did not carry this plasmid whereas virulent strains did [10]. This accomplishment allowed the authors to propose the hypothesis that ‘The tumor-inducing principle (Braun 1947) in crown-gall inducing Agrobacterium strains is carried by one or several large plasmids of various lengths’. The next year witnessed intense activity during which this hypothesis was tested. Specifically the loss of virulence via the heat-inactivation process described by Hamilton was correlated with the loss of the large plasmid and the transfer of virulence into avirulent strains, using the methods of Kerr, was correlated with the gain of this plasmid [11–13]. In agreement with Morel’s findings, if a plasmid specified, for example, production of nopaline by the tumor it also specified nopaline use by the bacterium. The conclusions were clear: a large plasmid, referred to as the Ti plasmid, specified tumor formation and opine production by the plant and opine use by the bacterium. Now the question became specific. Does the Ti plasmid produce a TIP and specify the type of opine produced by the tumor? Or is it, rather, responsible for the transfer of TIP and opine specification, encoded elsewhere on the bacterial genome, to the plant? One logical answer was that the plasmid was somehow transferred into the plant cell and carried out its activities in that environment. Although several different methodologies were used to test this hypothesis, solution hybridization studies in the mid 1970s to monitor for the presence of Ti plasmid sequences in DNA isolated from axenic crown gall tumors finally yielded the answer. In the first of these experiments, the Ti plasmid was radiolabeled and converted to single-strand form by denaturation. This was then mixed with a high concentration of sheared, denatured tumor DNA and the formation of double-stranded complexes containing the radiolabeled Ti plasmid DNA was monitored. If the tumor DNA contained a copy (or copies) of the Ti plasmid, then formation of radiolabeled, double-stranded DNA should occur more rapidly than in samples using nontransformed plant DNA. However, no evidence could be found for the presence of Ti plasmid sequences in tumor DNA [14]. Although these experiments showed that the entire Ti plasmid could not be incorporated into the tumor cell genome, they did not exclude the possibility that only a part of the plasmid was transferred into and/or retained in the transformed plant cell. The capacity to test this hypothesis was provided by the use of the recently discovered restriction enzymes. Chilton et al.[1] digested Ti plasmid DNA with SmaI yielding numerous different size DNA fragments that were then tested individually. Their prediction was as follows:‘… if only part of the plasmid genome is in the tumor, the reassociation rate of some fragments should be accelerated in the presence of tumor DNA, while other fragments should show no rate increase’. The results were striking …
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植物细胞信息内容的修改：R. Markham、D. R. Davies、D. A. Hopwood 和 R. W. Horne 编辑，阿姆斯特丹和纽约（1975 年），350 页，价格 24·50 美元。
DOI：
--
发表时间：
1976
期刊：
影响因子：
--
作者：
J. Callow
通讯作者：
J. Callow
影响因子：
3.2
作者：
B. Watson;T. C. Currier;M. Gordon;M. Chilton;E. Nester
通讯作者：
E. Nester
影响因子：
64.5
作者：
BARTON, KA;BINNS, AN;CHILTON, MD
通讯作者：
CHILTON, MD
DOI：
--
发表时间：
1984
期刊：
影响因子：
--
作者：
E. Nester;M. Gordon;R. Amasino;M. Yanofsky
通讯作者：
M. Yanofsky
DOI：
--
发表时间：
1942
期刊：
影响因子：
--
作者：
P. R. White;A. C. Braun
通讯作者：
A. C. Braun