1981
DOI: 10.1007/978-3-642-68120-2_3
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Replication Signals in Prokaryotic DNA

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1982
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Cited by 12 publications
(5 citation statements)
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“…The origin DNA binding activity of 5-6S T antigen was -10-fold greater than that of the 14-16S subclass (Figure 3). However, the affinity of 14-16S T antigen for origin DNA was equal to or Tjian, 1978Tjian, ,1979 Myers and Tjian, 1980;(c) McKay, 1981; McKay and DiMaio, 1981; (e) Shalloway et al, 1980;(f) Tegtmeyer et al, 1981;(g) DiMaio and Nathans, 1980). slightly greater than that of the 5-6S form ( Figure 4A), but its affinity for cellular DNA was much greater (Figure 4B,C).…”
Section: Discussionmentioning
confidence: 92%
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“…The origin DNA binding activity of 5-6S T antigen was -10-fold greater than that of the 14-16S subclass (Figure 3). However, the affinity of 14-16S T antigen for origin DNA was equal to or Tjian, 1978Tjian, ,1979 Myers and Tjian, 1980;(c) McKay, 1981; McKay and DiMaio, 1981; (e) Shalloway et al, 1980;(f) Tegtmeyer et al, 1981;(g) DiMaio and Nathans, 1980). slightly greater than that of the 5-6S form ( Figure 4A), but its affinity for cellular DNA was much greater (Figure 4B,C).…”
Section: Discussionmentioning
confidence: 92%
“…The 5-6S form of T antigen appears to bind more 'efficiently' to the viral origin region than the 14-16S form Gidoni et al, 1982; Figure 1). However, the affinity of 14-16S T antigen for origin DNA was equal to or Tjian, 1978Tjian, ,1979 Myers and Tjian, 1980;(c) McKay, 1981; McKay and DiMaio, 1981; (e) Shalloway et al, 1980;(f) Tegtmeyer et al, 1981;(g) DiMaio and Nathans, 1980). The origin DNA binding activity of 5-6S T antigen was -10-fold greater than that of the 14-16S subclass ( Figure 3).…”
Section: Discussionmentioning
confidence: 94%
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“…The initiation of replication on the two strands of ori sequences Since replication initiation may be due to two different enzymes, it is conceivable that the frequency of replication initiation is different on the two strands, and also that initiation on the 'non-r strand' requires previous opening of cluster C by transcripts and/or nascent DNA chains copied on the 'r strand'. Incidentally, this explanation (inspired by the transcriptional activation proposed for other genomes; Hobom, 1981), suggests that the inactivation of the r sequence by the insertion of cluster -y may also block replication using the 'non-r strand' as template. In any case, if replication of one strand lags behind that of the other, the replication of the lagging strand would become the rate-limiting factor in the replication of the tandem repeat units of spontaneous petite genome.…”
Section: Discussionmentioning
confidence: 99%
“…Most striking is the asymmetry seen in the left and right arm bp frequency profiles ( Fig 2 ). We favour the idea that this asymmetry reflects frequent failure of bidirectionality, such that c2 and c3 occasionally replicate by reverting to the unidirectional replication mode that presumably characterized their plasmid ancestors [ 57 ]. This observation has an important corollary—that a crucial component of the transition of a replicon from low-copy number plasmid to chromosome lifestyle is acquisition of the ability to replicate bidirectionally, thus halving the replication time and allowing the progressively expanding replicon to be replicated within the cell cycle.…”
Section: Discussionmentioning
confidence: 99%