Muster C J, Shapiro J A, MacHattie L A
Proc Natl Acad Sci U S A. 1983 Apr;80(8):2314-7. doi: 10.1073/pnas.80.8.2314.
Donor DNA molecules carrying Tn1 or Tn3 deletion mutants do not need to replicate in order to participate in replicon fusion recombination events during which the Tn1/Tn3 element is duplicated. We have assayed Tn1 delta Ap-mediated replicon fusion events involving plasmid R388 and the bacteriophage lambda-derived plasmid p lambda CM, and we find that the role of the recipient molecule is distinct. When p lambda CM carries Tn1 delta Ap, replicon fusion occurs in more than 1% of all cells assayed, whether or not p lambda CM::Tn1 delta Ap can replicate. In contrast, when R388 carries Tn1 delta Ap, replicon fusion occurs only when the p lambda CM target can replicate. Blocks to p lambda CM replication by prophage repressor or amber mutations of the O and P cistrons reduce replicon fusion so that it occurs in less than 1 out of 10(5) cells assayed.
携带Tn1或Tn3缺失突变体的供体DNA分子在参与复制子融合重组事件(在此期间Tn1/Tn3元件会被复制)时无需进行复制。我们已经检测了涉及质粒R388和噬菌体λ衍生质粒pλCM的Tn1ΔAp介导的复制子融合事件,并且我们发现受体分子的作用是不同的。当pλCM携带Tn1ΔAp时,无论pλCM::Tn1ΔAp是否能够复制,在所有检测的细胞中超过1%会发生复制子融合。相比之下,当R388携带Tn1ΔAp时,只有当pλCM靶标能够复制时才会发生复制子融合。前噬菌体阻遏物对pλCM复制的阻断或O和P顺反子的琥珀突变会减少复制子融合,以至于在每10⁵个检测细胞中发生的复制子融合不到1个。